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-   -   Change in Erectile Function after Stopping Clomid and Pramipexole (http://thinksteroids.com/forum/mens-health-forum/change-erectile-function-after-134311034.html)

SacToSD 09-02-2011 05:24 PM

Change in Erectile Function after Stopping Clomid and Pramipexole
 
I wanted to post this and seek advice/input from all of you on my current situation.

I attempted a clomiphene restart lasting 10 weeks at 50 mg/day, and during that time, I was treating my erectile dysfunction with pramipexole and cialis.

I got off of clomiphene and pramipexole 1 month ago.

During the 1st week off of clomiphene and pramipexole, I was having good erections taking 5 mg of cialis, per day.

Now, 1 month later, I am having consistent difficulties achieving erections with 20 mg cialis, per day.

However, I have started having morning erections these last 2 weeks, after not having them for over 1 year.

My lab work on August 1st, immediately after stopping clomiphene and pramipexole, was:

Total Testosterone: 875
Estrogen 48.9 (10-50, 20-30 recommended)
Prolactin 14.8 (4-15)
LH 6.5 (~5-15)
FSH 2.4 (~5-15)

I would like to order a new panel of labs, and want to include SHBG and DHT, in addition to an ultra-sensitive estradiol, free and total testosterone, prolactin, LH, and FSH.

I would like to not become dependent on TRT if at all possible.

Thanks

zkt 09-02-2011 06:19 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Quote:

Originally Posted by SacToSD (Post 778922)
I wanted to post this and seek advice/input from all of you on my current situation.

I attempted a clomiphene restart lasting 10 weeks at 50 mg/day, and during that time, I was treating my erectile dysfunction with pramipexole and cialis.

I got off of clomiphene and pramipexole 1 month ago.

During the 1st week off of clomiphene and pramipexole, I was having good erections taking 5 mg of cialis, per day.

Now, 1 month later, I am having consistent difficulties achieving erections with 20 mg cialis, per day.

However, I have started having morning erections these last 2 weeks, after not having them for over 1 year.

My lab work on August 1st, immediately after stopping clomiphene and pramipexole, was:

Total Testosterone: 875
Estrogen 48.9 (10-50, 20-30 recommended)
Prolactin 14.8 (4-15)
LH 6.5 (~5-15)
FSH 2.4 (~5-15)

I would like to order a new panel of labs, and want to include SHBG and DHT, in addition to an ultra-sensitive estradiol, free and total testosterone, prolactin, LH, and FSH.

I would like to not become dependent on TRT if at all possible.

Thanks

Not sure what I could advise. How do you feel the prami effected you? The effect of the parasympathetic nervous system on wood is greatly under-sestimated around here.

SacToSD 09-02-2011 06:37 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Quote:

Originally Posted by zkt (Post 778933)
Not sure what I could advise. How do you feel the prami effected you? The effect of the parasympathetic nervous system on wood is greatly under-sestimated around here.

The pramipexole didn't seem to have a noticeable effect in terms of libido or erectile function. I used it for 4 months at 0.5 mg/day, in one dose, in the morning, after titrating up for 2 weeks.

I tried intermittent doses of pramipexole during the second week of august when I noticed the beginnings of increased erectile dysfunction, and to my dismay, my normal dose made me a zombie. This would seem to indicate that my dopaminergic neurons had upregulated, as evidenced by my reduced tolerance.

Since August 6th I have been on Wellbutrin, aka burpopion, a norepinephrine/dopamine reuptake inhibitor. I started this at the request of my primary care physician to combat the extreme depression I was experiencing after getting off of clomiphene and pramipexole.

If what I'm thinking is correct, my norepinephrine is high, my dopamine is low, and my estrogen is high or low.

Here's my research.

Premise: High norephinephrine can cause ED
Support:
"High norepinephrine levels (or relatively high norepinephrine levels compared to the other neurotransmitters) can cause erectile dysfunction (chronic or otherwise).

Norepinephrine is the primary signal in the brain for stress. It is a excitatory neurotransmitter. It keeps a person awake. It can help improve attention. It causes an increase in ACTH production, which then drives adrenal hormone production. A spike of norepinephrine triggers orgasm/ejaculation in men. Norepinephrine is the primary chemical messenger of the sympathetic nervous system (the system that responds to fight-or-flight, stressful situations).

When a person has chronically high norepinephrine, it can cause anxiety or irritability. It can eventually cause adrenal depletion, fatigue, or frank adrenal insufficiency. This can then lead to erectile dysfunction, loss of libido, sexual dysfunction.

To keep norepinephrine levels high, the brain may have to lower the production of dopamine, which can lead to loss of libido and erectile dysfunction. Lowered dopamine production, itself, can reduce testosterone production (though high norepinephrine can raise it - causing a wash if the balance is maintained). Lower testosterone can lead to erectile dysfunction. Lowered testosterone production can lead to insulin resistance and further metabolic cascades that can cause erectilve dysfunction and lack of libido.

Chronically high norepinephrine production in the absence of other neurotransmitter, hormone, cytokine problems, can lead to premature ejaculation - since it doesn't take much to get a higher norepinephrine spike to trigger ejaculation.

Chronically high norepinephrine can raise blood pressure. This leads to long-term consequences, including renal dysfunction and erectile dysfunction.

What can be done is to either directly address the high norepinephrine production (e.g. with a serotonergic, anxiolytic, mood stabilizing, beta-blocking medication or others), or treat the consequences - such as adrenal fatigue (where the higher cortisol levels from treatment can help reduce via a feedback loop in the brain to lower CRH production, to lower norepinephrine levels), or treat the underlying cause of higher norepinephrine levels (which can include psychological stress, trauma, mental illness, thyroid dysfunction, hypogonadism, insulin resistance, infection or other chronic physical illness, etc.). In a way, a global treatment once assessment occurs, needs to be done. I usually don't see a single substance (drug, hormone, or nutrient, or even herb) working. There are many entrypoints to dysfunction when a single hormone/neurotransmitter is out of whack in function. What I usually see are multiple hormone/neurotransmitter/cytokine problems as a consequence.

http://forum.mesomorphosis.com/mens-...#ixzz1WpzAU1ou

__________________________________________________ ___________________

Premise: Impaired Nervous System Function re: norepinephrine
Support:
"OBJECTIVES:
To examine and compare the courses of norepinephrine (NE) and epinephrine (E) plasma levels in the systemic and cavernous blood taken during different penile conditions from healthy men and a group of patients with erectile dysfunction (ED). Knowledge concerning the neurophysiology of penile erection has improved tremendously during the past two decades. However, only few in vivo studies on human peripheral neurotransmission have been carried out to date.

METHODS:
Fifty-three healthy adult male subjects and 47 patients with ED of different etiologies were exposed to erotic stimuli to elicit penile tumescence and, in the group of healthy subjects, rigidity. Whole blood was simultaneously aspirated from the corpus cavernosum and the cubital vein during different penile conditions. Plasma levels of NE and E were determined by means of a radioimmunoassay.

RESULTS:
In the healthy subjects, a significant reduction of NE in cavernous plasma was detected from flaccidity (362 +/- 173 pg/mL) to rigidity (248 +/- 122 pg/mL), followed by an increase in the detumescence phase (336 +/- 199 pg/mL). Changes in NE levels in the peripheral plasma were less pronounced. Cavernous E levels significantly increased from flaccidity (47 +/- 41 pg/mL) to tumescence (130 +/- 106 pg/mL) and dropped from rigidity (113 +/- 67 pg/mL) to detumescence (76 +/- 57 pg/mL). The course of systemic E plasma levels was similar to that in the cavernous blood. In contrast, median NE levels in the systemic and cavernous blood of the ED group slightly increased from flaccidity to tumescence (from 199 +/- 88 pg/mL to 210 +/- 99 pg/mL and from 273 +/- 140 pg/mL to 278 +/- 118 pg/mL, respectively).

CONCLUSIONS:
In healthy men, penile erection is accompanied by a reduction of NE in the cavernous blood and a rise in E levels in the peripheral and cavernous blood. That NE levels in the cavernous and systemic blood increase during sexual arousal in patients with ED might be an indication of a somatic dysregulation in sympathetic transmission or alterations of NE reuptake mechanisms as a cause of impaired erectile function.

Cavernous and systemic plasma levels of norepinephri... [Urology. 2002] - PubMed - NCBI

Urology. 2002 Feb;59(2):281-6.
Becker AJ, Uckert S, Stief CG, Scheller F, Knapp WH, Hartmann U, Jonas U.

__________________________________________________ _____________

Conclusions:

If my morning erections serve to indicate a proper testosterone:estrogen ratio, and I'm getting morning erections consistently, then my testosterone:estrogen ratio is good.

If I'm failing to achieve good erections when desired, then that is a function of the nervous system, since we've eliminated the testosterone:estrogen ratio as a culprit.

My use of Wellbutrin, a norepinephrine reuptake inhibitor, may be contributing to my erectile dysfunction, since "alterations of NE reuptake mechanisms [can be]... a cause of impaired erectile function," (Becker, et all).


Planned course of action:
1. Stop taking Wellbutrin/bupropion
2. Monitor morning erections
3. Get blood test in 1 week for: total and free testosterone, ultra-sensitive estradiol (E2), prolactin, DHT, SHBG, LH, FSH, norepinephrine, dopamine.

SacToSD 09-02-2011 06:58 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
More support for increased norepinephrine hypothesis:

"In the flaccid state of the penis, frequent release of norepinephrine from sympathetic nerves contracts the arteries in the penis and also contracts the smooth muscles of the corpora cavernosum. Therefore, in the normal state, norepinephrine keeps the penis soft. A relative predominance of norepinephrine-induced contraction over nitric oxide-mediated relaxation may contribute to erectile dysfunction. Two amino acids phenylalanine and tyrosine, sold as supplements, are converted into dopamine. Dopamine, in turn, is converted into norepinephrine, and then epinephrine. The ingestion of these amino acids elevates dopamine and norepinephrine levels, and hence will lead to alertness and mood elevation and increased sexual interest. However, excess amounts of norepinephrine and epinephrine may make it difficult to have erections. In addition, high amounts raise blood pressure, increase heart rate, and cause anxiety, irritability, and insomnia. Yohimbe, the natural sex booster from Africa, facilitates erections by blocking the inhibitory action of norepinephrine on the penis."

Subjective support for norepinephrine hypothesis:
Over the last few weeks, since this whole problem has started, I've noticed that I've had increased shrinkage of the penis, as in, it's smaller than normal in the flaccid state, feels like I just got out of the pool. This would be symptomatic of high norepinephrine levels.

Plan: try using yohimbe.

zkt 09-02-2011 07:12 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Damn! Youve been doing your homework !
One problem is that serum levels dont reflect local brain levels of neurotransmitters, NE DA,etc.
To further complicate the matter, certain neurons in the brain secrete certain neurotransmitters and whose effect is only local. So you cant alter brain chemistry by changing systemic levels.
Abd the neurotransmiters do different things in different areas of the brain. Not th mention the many subsets of the basic receptors, The opiate receptors alone have 12 subclasses each having a bit different effect.
Bupropion is well known to not cause sexual side effects. To the contrary it often increases libido.
I totally agree that T and E must be in the proper ratio for the wood to work. For an erection to happen nitric oxide must increase to cause vasodialation in the cavernous vessels. NE is a vasoconstrictor via action on the Alpha2 receptors in the vascular endothelium. Its a very complicated mess and I fear that you are oversimplifing the system. But I hope you are in the right track.


Quote:

Originally Posted by SacToSD (Post 778946)
The pramipexole didn't seem to have a noticeable effect in terms of libido or erectile function. I used it for 4 months at 0.5 mg/day, in one dose, in the morning, after titrating up for 2 weeks.

I tried intermittent doses of pramipexole during the second week of august when I noticed the beginnings of increased erectile dysfunction, and to my dismay, my normal dose made me a zombie. This would seem to indicate that my dopaminergic neurons had upregulated, as evidenced by my reduced tolerance.

Since August 6th I have been on Wellbutrin, aka burpopion, a norepinephrine/dopamine reuptake inhibitor. I started this at the request of my primary care physician to combat the extreme depression I was experiencing after getting off of clomiphene and pramipexole.

If what I'm thinking is correct, my norepinephrine is high, my dopamine is low, and my estrogen is high or low.

Here's my research.

Premise: High norephinephrine can cause ED
Support:
"High norepinephrine levels (or relatively high norepinephrine levels compared to the other neurotransmitters) can cause erectile dysfunction (chronic or otherwise).

Norepinephrine is the primary signal in the brain for stress. It is a excitatory neurotransmitter. It keeps a person awake. It can help improve attention. It causes an increase in ACTH production, which then drives adrenal hormone production. A spike of norepinephrine triggers orgasm/ejaculation in men. Norepinephrine is the primary chemical messenger of the sympathetic nervous system (the system that responds to fight-or-flight, stressful situations).

When a person has chronically high norepinephrine, it can cause anxiety or irritability. It can eventually cause adrenal depletion, fatigue, or frank adrenal insufficiency. This can then lead to erectile dysfunction, loss of libido, sexual dysfunction.

To keep norepinephrine levels high, the brain may have to lower the production of dopamine, which can lead to loss of libido and erectile dysfunction. Lowered dopamine production, itself, can reduce testosterone production (though high norepinephrine can raise it - causing a wash if the balance is maintained). Lower testosterone can lead to erectile dysfunction. Lowered testosterone production can lead to insulin resistance and further metabolic cascades that can cause erectilve dysfunction and lack of libido.

Chronically high norepinephrine production in the absence of other neurotransmitter, hormone, cytokine problems, can lead to premature ejaculation - since it doesn't take much to get a higher norepinephrine spike to trigger ejaculation.

Chronically high norepinephrine can raise blood pressure. This leads to long-term consequences, including renal dysfunction and erectile dysfunction.

What can be done is to either directly address the high norepinephrine production (e.g. with a serotonergic, anxiolytic, mood stabilizing, beta-blocking medication or others), or treat the consequences - such as adrenal fatigue (where the higher cortisol levels from treatment can help reduce via a feedback loop in the brain to lower CRH production, to lower norepinephrine levels), or treat the underlying cause of higher norepinephrine levels (which can include psychological stress, trauma, mental illness, thyroid dysfunction, hypogonadism, insulin resistance, infection or other chronic physical illness, etc.). In a way, a global treatment once assessment occurs, needs to be done. I usually don't see a single substance (drug, hormone, or nutrient, or even herb) working. There are many entrypoints to dysfunction when a single hormone/neurotransmitter is out of whack in function. What I usually see are multiple hormone/neurotransmitter/cytokine problems as a consequence.

http://forum.mesomorphosis.com/mens-...#ixzz1WpzAU1ou

__________________________________________________ ___________________

Premise: Impaired Nervous System Function re: norepinephrine
Support:
"OBJECTIVES:
To examine and compare the courses of norepinephrine (NE) and epinephrine (E) plasma levels in the systemic and cavernous blood taken during different penile conditions from healthy men and a group of patients with erectile dysfunction (ED). Knowledge concerning the neurophysiology of penile erection has improved tremendously during the past two decades. However, only few in vivo studies on human peripheral neurotransmission have been carried out to date.

METHODS:
Fifty-three healthy adult male subjects and 47 patients with ED of different etiologies were exposed to erotic stimuli to elicit penile tumescence and, in the group of healthy subjects, rigidity. Whole blood was simultaneously aspirated from the corpus cavernosum and the cubital vein during different penile conditions. Plasma levels of NE and E were determined by means of a radioimmunoassay.

RESULTS:
In the healthy subjects, a significant reduction of NE in cavernous plasma was detected from flaccidity (362 +/- 173 pg/mL) to rigidity (248 +/- 122 pg/mL), followed by an increase in the detumescence phase (336 +/- 199 pg/mL). Changes in NE levels in the peripheral plasma were less pronounced. Cavernous E levels significantly increased from flaccidity (47 +/- 41 pg/mL) to tumescence (130 +/- 106 pg/mL) and dropped from rigidity (113 +/- 67 pg/mL) to detumescence (76 +/- 57 pg/mL). The course of systemic E plasma levels was similar to that in the cavernous blood. In contrast, median NE levels in the systemic and cavernous blood of the ED group slightly increased from flaccidity to tumescence (from 199 +/- 88 pg/mL to 210 +/- 99 pg/mL and from 273 +/- 140 pg/mL to 278 +/- 118 pg/mL, respectively).

CONCLUSIONS:
In healthy men, penile erection is accompanied by a reduction of NE in the cavernous blood and a rise in E levels in the peripheral and cavernous blood. That NE levels in the cavernous and systemic blood increase during sexual arousal in patients with ED might be an indication of a somatic dysregulation in sympathetic transmission or alterations of NE reuptake mechanisms as a cause of impaired erectile function.

Cavernous and systemic plasma levels of norepinephri... [Urology. 2002] - PubMed - NCBI

Urology. 2002 Feb;59(2):281-6.
Becker AJ, Uckert S, Stief CG, Scheller F, Knapp WH, Hartmann U, Jonas U.

__________________________________________________ _____________

Conclusions:

If my morning erections serve to indicate a proper testosterone:estrogen ratio, and I'm getting morning erections consistently, then my testosterone:estrogen ratio is good.

If I'm failing to achieve good erections when desired, then that is a function of the nervous system, since we've eliminated the testosterone:estrogen ratio as a culprit.

My use of Wellbutrin, a norepinephrine reuptake inhibitor, may be contributing to my erectile dysfunction, since "alterations of NE reuptake mechanisms [can be]... a cause of impaired erectile function," (Becker, et all).


Planned course of action:
1. Stop taking Wellbutrin/bupropion
2. Monitor morning erections
3. Get blood test in 1 week for: total and free testosterone, ultra-sensitive estradiol (E2), prolactin, DHT, SHBG, LH, FSH, norepinephrine, dopamine.


SacToSD 09-02-2011 07:27 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Quote:

Originally Posted by zkt (Post 778957)
Damn! Youve been doing your homework !

Bupropion is well known to not cause sexual side effects. To the contrary it often increases libido.
I totally agree that T and E must be in the proper ratio for the wood to work. For an erection to happen nitric oxide must increase to cause vasodialation in the cavernous vessels. NE is a vasoconstrictor via action on the Alpha2 receptors in the vascular endothelium. Its a very complicated mess and I fear that you are oversimplifing the system. But I hope you are in the right track.

It does seem oversimplified, yes. The reason I presumed that norepinephrine is high is due to the conversion of dopamine to norepinephrine, and the potential effects of using a dopamine agonist like pramipexole and the type of effects it might cause. In other words, using pramipexole may have downregulated my dopaminergic neurons, and now that I'm off of pramipexole, more dopamine is being produced since there is less dopaminergic activity at the neurons since there are fewer receptors. That creates an excess of dopamine, and therefore an increase in norepinephrine, atypical of the results people using Wellbutrin experience re: sexual side effects, or lack thereof.

I may be on the wrong track, but I'm on a track, regardless. I'm going to try some yohimbe, since that seems to negate the effects of norepinephrine in regard to erectile function. This should either support or refute my hypothesis.

Thanks for the feedback, so far.

zkt 09-03-2011 07:37 AM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
What you say does sound reasonable. Keep us appraised of your experiments. :)

4-chloro 09-03-2011 04:02 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Receptor down regulation from only 500mcg of pramipexole is highly unlikely, and usually occurs from acute floods of neurotransmitters such as those caused by pyschotropic drugs like methamphetamine and MDMA. MDMA for example can cause serotonin receptor downregulation for 7 years after a single dose, as it releases the equivalent of 6 years of serotonin at once.

Pramipexole might cause your brain to produce less dopamine or upregulate it's oxidative proteins as it is essentially acquiring it exogenously from the mirapex.

Your elevated prolactin level could be a sign of this. It is also important to keep in mind that wellbutrin does not lower prolactin as it doesn't target the reuptake of a large enough percentage of dopamine receptors in the brain, it also however does not raise it. NE's effect on the dopamine transporter pump is statistically insignificant in most cases.

As stated before, this is all a summary of a largely complex process. It is not likely that NE alone can cause ED, but more in the ratio of NT's. Methamphetamine for example will cause a ~1200% increase in dopamine, and a ~500% increase in NE (thus raising TSH, LH, FSH and cortisol) but produces a wildly increased libido and sexual performance.

I would put money down that a low dose of Dextroamphetamine (Dexedrine) would significantly improve your case, and would help with Mirapex "withdrawal".

It would also be wise to address the prolactin and estradiol issue.

SacToSD 09-03-2011 06:09 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Quote:

Originally Posted by zkt (Post 779018)
What you say does sound reasonable. Keep us appraised of your experiments. :)

Thanks, I will.

I don't like clutching at straws, but if I clutch at enough of them, maybe something will pan out.

I'm going in for a full blood panel on Monday or Tuesday.

Quote:

Originally Posted by 4-chloro (Post 779099)
Receptor down regulation from only 500mcg of pramipexole is highly unlikely, and usually occurs from acute floods of neurotransmitters such as those caused by pyschotropic drugs like methamphetamine and MDMA. MDMA for example can cause serotonin receptor downregulation for 7 years after a single dose, as it releases the equivalent of 6 years of serotonin at once.

Pramipexole might cause your brain to produce less dopamine or upregulate it's oxidative proteins as it is essentially acquiring it exogenously from the mirapex.

Your elevated prolactin level could be a sign of this. It is also important to keep in mind that wellbutrin does not lower prolactin as it doesn't target the reuptake of a large enough percentage of dopamine receptors in the brain, it also however does not raise it. NE's effect on the dopamine transporter pump is statistically insignificant in most cases.

As stated before, this is all a summary of a largely complex process. It is not likely that NE alone can cause ED, but more in the ratio of NT's. Methamphetamine for example will cause a ~1200% increase in dopamine, and a ~500% increase in NE (thus raising TSH, LH, FSH and cortisol) but produces a wildly increased libido and sexual performance.

I would put money down that a low dose of Dextroamphetamine (Dexedrine) would significantly improve your case, and would help with Mirapex "withdrawal".

It would also be wise to address the prolactin and estradiol issue.

Great post, 4-chloro. What compound are you referring to in your name that has chlorine on c4?

You're probably right. I did some digging into Wellbutrin research, and found this study:

Effects of Bupropion Sustained-Release on Sexual Functioning and Nocturnal Erections in Healthy Men
Labbate, Lawrence A. MD*‡; Brodrick, Peter S. MD*‡; Nelson, Robert P. MD†‡; Lydiard, R. Bruce MD, PhD*; Arana, George W. MD*‡

"Many antidepressants are known to cause adverse sexual effects. Bupropion is an antidepressant with fewer reported adverse sexual effects. Studies of sexual side effects are often confounded by psychiatric and medical conditions affecting sexual function. In this study, the effects of bupropion on subjective and objective sexual functioning were measured in healthy men. Thirteen men without psychiatric or medical illness completed a 2-week, placebo-controlled, double-blind, crossover trial of bupropion sustained-release 300 mg/day. Subjects had a 1-week washout period between trials. Sexual function was measured using a validated, self-administered questionnaire and the RigiScan, an instrument measuring nocturnal penile tumescence and rigidity. No differences were found in self-reported sexual function, number of erections, total erection time, or penile rigidity in subjects taking bupropion compared with those taking placebo or baseline. These findings support that bupropion does not have subjective adverse sexual side effects and does not affect nocturnal erections in healthy men."

So, if Wellbutrin doesn't help anything but the desire component, then I'm getting off, to find a better starting point for this puzzle of ED/libido that I'm trying to solve.

You're probably right about the estradiol and prolactin, too.

On that topic, I strongly suspect that my estradiol is causing problems. When I was treating with clomiphene, it may have caused an estrogen rebound when my labs showing high estradiol were taken. When I treated it with Arimidex for ~10 days, my estrogen went too low and I was having all of the classic signs and symptoms of low estrogen (joint pain, complete ED that wouldn't correct with PDE5 inhibitors [Cialis]). I stopped taking the Arimidex 2 weeks ago. Therefore, there might be lingering effects of low (or high) estradiol contributing to my altered erectile capacity.

If my labs on Monday show high or low estradiol, I'll know what is going on in that regard.

Hopefully, with getting my DHT, SHBG, free and total testosterone, ultra sensitive estradiol, prolactin, we can find out more.

I wish that I could order my own labs. That would make this so much easier.

4-chloro 09-03-2011 10:11 PM

Re: Change in Erectile Function after Stopping Clomid and Pramipexole
 
Quote:

Originally Posted by SacToSD (Post 779112)
Thanks, I will.

I don't like clutching at straws, but if I clutch at enough of them, maybe something will pan out.

I'm going in for a full blood panel on Monday or Tuesday.



Great post, 4-chloro. What compound are you referring to in your name that has chlorine on c4?

You're probably right. I did some digging into Wellbutrin research, and found this study:

Effects of Bupropion Sustained-Release on Sexual Functioning and Nocturnal Erections in Healthy Men
Labbate, Lawrence A. MD*‡; Brodrick, Peter S. MD*‡; Nelson, Robert P. MD†‡; Lydiard, R. Bruce MD, PhD*; Arana, George W. MD*‡

"Many antidepressants are known to cause adverse sexual effects. Bupropion is an antidepressant with fewer reported adverse sexual effects. Studies of sexual side effects are often confounded by psychiatric and medical conditions affecting sexual function. In this study, the effects of bupropion on subjective and objective sexual functioning were measured in healthy men. Thirteen men without psychiatric or medical illness completed a 2-week, placebo-controlled, double-blind, crossover trial of bupropion sustained-release 300 mg/day. Subjects had a 1-week washout period between trials. Sexual function was measured using a validated, self-administered questionnaire and the RigiScan, an instrument measuring nocturnal penile tumescence and rigidity. No differences were found in self-reported sexual function, number of erections, total erection time, or penile rigidity in subjects taking bupropion compared with those taking placebo or baseline. These findings support that bupropion does not have subjective adverse sexual side effects and does not affect nocturnal erections in healthy men."

So, if Wellbutrin doesn't help anything but the desire component, then I'm getting off, to find a better starting point for this puzzle of ED/libido that I'm trying to solve.

You're probably right about the estradiol and prolactin, too.

On that topic, I strongly suspect that my estradiol is causing problems. When I was treating with clomiphene, it may have caused an estrogen rebound when my labs showing high estradiol were taken. When I treated it with Arimidex for ~10 days, my estrogen went too low and I was having all of the classic signs and symptoms of low estrogen (joint pain, complete ED that wouldn't correct with PDE5 inhibitors [Cialis]). I stopped taking the Arimidex 2 weeks ago. Therefore, there might be lingering effects of low (or high) estradiol contributing to my altered erectile capacity.

If my labs on Monday show high or low estradiol, I'll know what is going on in that regard.

Hopefully, with getting my DHT, SHBG, free and total testosterone, ultra sensitive estradiol, prolactin, we can find out more.

I wish that I could order my own labs. That would make this so much easier.

I would make a suggestion of Aromasin Vs Arimidex. Although I don't have any studies in bag o' tricks to support it (If people would like me to source more I can), I've heard it stated that Aromasin doesn't effect testosterone's aromatisation to estrogen in the brain, nearly as much as other non-steroidal AI's. Anecdotal evidence supports that it has a lowered negative effect on sex drive, and if you search pub med you can find evidence that it has lowered effects on cholesterol.

It can also be noted that daily dosing may not be necessary at all:





Eur J Endocrinol. 2008 May;158(5):741-7.
Letrozole once a week normalizes serum testosterone in obesity-related male hypogonadism.
Loves S, Ruinemans-Koerts J, de Boer H.
Source

Department of Internal Medicine, Ziekenhuis Rijnstate, Wagnerlaan 55, 6800 TA Arnhem, The Netherlands.
Abstract
OBJECTIVE:

Isolated hypogonadotropic hypogonadism (IHH) is frequently observed in severely obese men, probably as a result of increased estradiol (E(2)) production and E(2)-mediated negative feedback on pituitary LH secretion. Aromatase inhibitors can reverse this process. This study evaluates whether letrozole once a week can normalize serum testosterone in severely obese men and maintain its long term effect.
DESIGN:

Open, uncontrolled 6-month pilot study in 12 severely obese men (body mass index>35.0 kg/m(2)) with obesity-related IHH and free testosterone levels <225 pmol/l, treated with 2.5 mg letrozole once a week for 6 months.
RESULTS:

Six weeks of treatment reduced total E(2) from 123+/-11 to 58+/-7 pmol/l (P<0.001, mean+/-s.e.m.), and increased serum LH from 4.4+/-0.6 to 11.1+/-1.5 U/l (P<0.001). Total testosterone rose from 5.9+/-0.5 to 19.6+/-1.4 nmol/l (P<0.001), and free testosterone from 163+/-13 to 604+/-50 pmol/l (P<0.001). Total testosterone rose to within the normal range in all subjects, whereas free testosterone rose to supraphysiological levels in 7 out of 12 men. The testosterone and E(2) levels were stable throughout the week and during the 6-month treatment period.
CONCLUSION:

Letrozole 2.5 mg once a week produced a sustained normalization of serum total testosterone in obese men with IHH. However, free testosterone frequently rose to supraphysiological levels. Therefore, a starting dose <2.5 mg once a week is recommended.





All the AI's have similar half lives, so it would be safe to extrapolate this study to include aromasin and arimidex. 2.5mg of letrozole will reduce estrogen only slightly more than .5mg of letrozole or less. Similar to how 1mg of arimidex will lower estrogen only slightly more than .5mg of arimidex. I'm not sure why this occurs in males, but it could be because a saturation point of aromatase inhibition is reached with each drug as each has differing affinities to the aromatase enzyme.

This could explain why even a low dose of arimidex slaughtered your estradiol. I would (in an unprofessional opinion) suggest 12.5mg of aromasin on Monday and Thursday to start, and the dose can easily be adjusted. 25mg of aromasin will lower estradiol levels a similar amount as 2.5mg of letrozole, so less than 25mg a week will most likely be sufficient, but in order to fine tune it you'll have to get your estradiol retested until the desired dose is found.

Bloodwork is easiest when you ask your physician for a number of standing orders, for example you could ask for 8 standing orders to test:

DHT
Free/TT
Estradiol
Prolactin
LH
FSH
ACTH

That way you can go into the lab whenever you want and get your blood drawn (depending on the length of the order), the results will get sent to your physician and they can then call/email you the results.

To address the issue of prolactin (possibly the most irritating hormone in the male system) I would suggest (if possible) to get back on Mirapex, and take .75mg (half of a 1.5mg tab) 3 times a day. You'll have to work up to it as it can cause nausea and sedation, but it will subside. Your prolactin level will eventually drop, in which case you can stay on the Mirapex, or very very slowly taper off of it, along with 800mg of Vitex taken 1-2x daily. I would say .25mg every two weeks would be a reasonable reduction. It is my belief that most physicians take people off of psychotropic drugs much too quickly, as you've essentially been dependent on them 24/7 for months or even years. Wellbutrin for example inhibits the re-uptake of dopamine at the synapses, guess what drugs also do the same? Cocaine, Amphetamines etc.

I will also note that I never noticed any benefit from mirapex until I was taking it in 3 divided doses, however, my ADHD prescription augments the sedation piece. But even on days I do not take stimulants, I found the sedation to slowly subside after a few weeks.

The 4-chloro refers to Oral Turinabol (4-chlorodehydromethyltestosterone) :)


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