How does Pramipexole make you "feel?"

[RaveHead]

Yes. We all know that Prami is a dopamine agonist that causes a reduction in prolactin levels. That's great. I just got some, "in case of emergency" during my Deca cycle. But how has it made everyone "feel?" Do you notice any difference in your mood, sex drive, energy, aggression, etc.?

 

[Docd187123]

Yes. We all know that Prami is a dopamine agonist that causes a reduction in prolactin levels. That's great. I just got some, "in case of emergency" during my Deca cycle. But how has it made everyone "feel?" Do you notice any difference in your mood, sex drive, energy, aggression, etc.?

I can't say Ive noticed any mood benefits but refractory period is shortened. You'll also know if you took too much bc you'll feel like shit.

Edit* that's not to say I'm recommending it's use unless warranted.

 

[Bradly]

the first time I tried it I felt like shit, totally killed my appetite. each successive dose has gotten better though. slight libido increase,maybe mood improvement.

 

[RaveHead]

Yeah I often hear of the nausea and other GI side effects. An overload of the dopaminergic system causes this. Prami is a dopamine agonist. I often use the medication Reglan to treat the nausea I experience from my "sliding hiatal hernia," as diagnosed by my Gastroenterologist. Reglan is actually a dopamine antagonist. That is why there is a negative interaction between Reglan and Prami - they oppose each other. But taking Reglan as I usually do, would prevent the Prami induced GI upset. The question is, what is the right balance of doses between the two drugs to keep the nausea out but keep the positive effects of the Prami in. So now that we have the dopaminergic sides under control (with Reglan), then we are interested in the Prolactin benefits. You mentioned the shortened refractory period while of Prami, based on the idea that Prolactin increases post-orgasm in an attempt to cool us down after intercourse. But if you're making a "night of it" then by all means keep it going.

Some comment on the "lethargic" feeling caused by the Prami. Do you all have a comment on that particular side effect? Is it somehow modulated by the circadian rhythms involving lower/higher levels of dopamine, or is a different mechanism involved in this?

 

[PenisSurfer]

Some comment on the "lethargic" feeling caused by the Prami. Do you all have a comment on that particular side effect? Is it somehow modulated by the circadian rhythms involving lower/higher levels of dopamine, or is a different mechanism involved in this?

Why would that even matter?

 

[Michael Scally MD]

Worthless Bro BS

 

[Nutpuncher]

Why did you choose prami over caber? The reason why I ask is because I was also have Deca on deck and was recommend to take caber if needed.

 

[ironwill1951]

@Michael Scally MD I have been reading up on it a bit , im not sure what to think are you saying its bro science ?

Worthless Bro BS

 

[Docd187123]

Why did you choose prami over caber? The reason why I ask is because I was also have Deca on deck and was recommend to take caber if needed.

You need to control estrogen. Forget about prami and caber for now. Worry about your AI, E2, and bloodwork.

 

[Docd187123]

@Michael Scally MD I have been reading up on it a bit , im not sure what to think are you saying its bro science ?

That 19-nors are the reason for prolactin increases.

Sodi R, Fikri R, Diver M, Ranganath L, Vora J. Testosterone replacement-induced hyperprolactinaemia: case report and review of the literature. Ann Clin Biochem 2005;42(Pt 2):153-9.

Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy. We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.


Gill-Sharma MK. Prolactin and male fertility: the long and short feedback regulation. Int J Endocrinol 2009;2009:687259.

In the last 20 years, a pituitary-hypothalamus tissue culture system with intact neural and portal connections has been developed in our lab and used to understand the feedback mechanisms that regulate the secretions of adenohypophyseal hormones and fertility of male rats. In the last decade, several in vivo rat models have also been developed in our lab with a view to substantiate the in vitro findings, in order to delineate the role of pituitary hormones in the regulation of fertility of male rats. These studies have relied on both surgical and pharmacological interventions to modulate the secretions of gonadotropins and testosterone. The interrelationship between the circadian release of reproductive hormones has also been ascertained in normal men. Our studies suggest that testosterone regulates the secretion of prolactin through a long feedback mechanism, which appears to have been conserved from rats to humans. These studies have filled in a major lacuna pertaining to the role of prolactin in male reproductive physiology by demonstrating the interdependence between testosterone and prolactin. Systemic levels of prolactin play a deterministic role in the mechanism of chromatin condensation during spermiogenesis.


Gillam MP, Middler S, Freed DJ, Molitch ME. The novel use of very high doses of cabergoline and a combination of testosterone and an aromatase inhibitor in the treatment of a giant prolactinoma J Clin Endocrinol Metab 2002;87(10):4447-51.

Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia. A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 micro g/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 micro g/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 micro g/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.


Prior JC, Cox TA, Fairholm D, Kostashuk E, Nugent R. Testosterone-related exacerbation of a prolactin-producing macroadenoma: possible role for estrogen. J Clin Endocrinol Metab 1987;64(2):391-4.

Men with PRL-producing macroadenomas often present with hypogonadism and impotence. This report documents exacerbation of a PRL-secreting tumor after two separate 200-mg testosterone enanthate (T) injections despite continued bromocriptine (BRC) therapy. A 37-yr-old man with a 60-mm invasive tumor and a serum PRL level of 13,969 +/- 332 ng/ml (mean +/- SD) responded to BRC therapy with rapid disappearance of visual field defect, headache, and facial pain as well as decrease in serum PRL to 5,103 +/- 1,446 ng/ml. T injection was followed by severe headache, facial pain, and increase in PRL to 13,471 ng/ml. Visual field deterioration and increased tumor size (height, 40-43 mm) by computed tomography were documented. A relationship between T injection and exacerbation of the prolactinoma was not recognized until after a second T injection 3 months later. After that therapy, baseline PRL increased from 6,900 to 12,995 ng/ml. The hypothesis that T was aromatized to estradiol, directly stimulating lactotrophs, was supported by an increase in serum estradiol from 24 to 51 pg/ml after the second T injection. Although T treatment is accepted as appropriate therapy for hypogonadism in men with prolactinomas, it may not only interfere with the response of the tumor to BRC therapy, but even stimulate tumor growth and secretion.

 

[RaveHead]

Why would that even matter?

If I understood the mechanism behind the lethargy caused by the Prami, I might be able to counteract that side effect with something.

Thanks Doc for your input/references. Question. Do you have such posts by people like Michael Scally bookmarked on your computer or are you searching on Meso in a certain way. My personal search results on this sight always come back screwy. One comment I noticed in that research was that the estrogen stemming from the exogenous testosterone caused feedback to increase the production of Prolactin. That is sensible.

 

[Michael Scally MD]

That 19-nors are the reason for prolactin increases.

Someone here with a prolactinoma! Are we talking testosterone! Not.

Also, while 19-nor do aromatize, their metabolites are not that effective at the ER.

Aromatase: 17β -TBOH and other C19 norandrogens are reported to not be substrates for the aromatase enzyme and to be relatively non-estrogenic; although some debate exists regarding 19-nortestosterone to undergo aromatization and induce estrogenic effects. In vitro bioassays and cell culture experiments demonstrate that 17β - TBOH and its metabolites have a very low binding affinity for ERs and have low estrogenic activity with approximately 20% of the efficacy of E2.

Trenbolone - A summary from the article, "Yarrow JF, McCoy SC, Borst SE. Tissue selectivity and potential clinical applications of trenbolone (17[beta]-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity. Steroids. Tissue selectivity and potential clinical applications of trenbolone (17β-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity

In the patients I have treated on a 19-nor alone [ND & Tren], there has been NO rise in Prolactin. I would like to see the evidence before jumping on a dopamine agonist, but I recognize that is not how most go about this!!! Bro BS!

I know of but a few studies looking at this effect. These are not great studies, but would like to see any others.

Maeda Y, Nakanishi T, Ozawa K, et al. Anabolic steroid-associated hypogonadism in male hemodialysis patients. Clin Nephrol 1989;32:198-201. Anabolic steroid-associated hypogonadism in male hemodialysis patients. - PubMed - NCBI

Hypogonadism in male hemodialysis patients has been previously reported. However, its precise pathogenesis has not yet been clarified. Mepitiostane and nandrolone decanoate are anabolic steroids prescribed for uremic anemia, and those may possibly exacerbate uremic gonadal damage. We studied the influences of these steroids on male gonadal function. Seventy-six hemodialysis patients were selected and examined for levels of luteinizing hormone (LH), follicular stimulating hormone (FSH), total testosterone, and prolactin. Twenty-three patients who received anabolic steroids showed lower testosterone values (205.2 +/- 35.6 ng/dl) than did patients without these steroids (449.7 +/- 21.3 ng/dl). Gonadotropins and prolactin showed no significant differences between the patients with and without the steroids. The testosterone values of three patients with mepitiostane increased after they stopped taking steroids. One patient suffering from complete aspermia recovered (sperm count: 0/ml to 1300 x 10(4)/ml) after discontinuation of mepitiostane and administration of human chorionic gonadotropin (HCG). This clinical study suggests that some anabolic steroids play a role in uremic hypogonadism; thus mepitiostane or its analogues should be carefully prescribed for young male patients.


Donaldson IA, Hart IC, Heitzman RJ. Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol. Res Vet Sci 1981;30(1):7-13. Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with ... - PubMed - NCBI

The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.

 

[Docd187123]

Someone here with a prolactinoma! Are we talking testosterone! Not.

Also, while 19-nor do aromatize, their metabolites are not that effective at the ER.

Aromatase: 17β -TBOH and other C19 norandrogens are reported to not be substrates for the aromatase enzyme and to be relatively non-estrogenic; although some debate exists regarding 19-nortestosterone to undergo aromatization and induce estrogenic effects. In vitro bioassays and cell culture experiments demonstrate that 17β - TBOH and its metabolites have a very low binding affinity for ERs and have low estrogenic activity with approximately 20% of the efficacy of E2.

Trenbolone - A summary from the article, "Yarrow JF, McCoy SC, Borst SE. Tissue selectivity and potential clinical applications of trenbolone (17[beta]-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity. Steroids. Tissue selectivity and potential clinical applications of trenbolone (17β-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity

In the patients I have treated on a 19-nor alone [ND & Tren], there has been NO rise in Prolactin. I would like to see the evidence before jumping on a dopamine agonist, but I recognize that is not how most go about this!!! Bro BS!

I know of but a few studies looking at this effect. These are not great studies, but would like to see any others.

Maeda Y, Nakanishi T, Ozawa K, et al. Anabolic steroid-associated hypogonadism in male hemodialysis patients. Clin Nephrol 1989;32:198-201. Anabolic steroid-associated hypogonadism in male hemodialysis patients. - PubMed - NCBI

Hypogonadism in male hemodialysis patients has been previously reported. However, its precise pathogenesis has not yet been clarified. Mepitiostane and nandrolone decanoate are anabolic steroids prescribed for uremic anemia, and those may possibly exacerbate uremic gonadal damage. We studied the influences of these steroids on male gonadal function. Seventy-six hemodialysis patients were selected and examined for levels of luteinizing hormone (LH), follicular stimulating hormone (FSH), total testosterone, and prolactin. Twenty-three patients who received anabolic steroids showed lower testosterone values (205.2 +/- 35.6 ng/dl) than did patients without these steroids (449.7 +/- 21.3 ng/dl). Gonadotropins and prolactin showed no significant differences between the patients with and without the steroids. The testosterone values of three patients with mepitiostane increased after they stopped taking steroids. One patient suffering from complete aspermia recovered (sperm count: 0/ml to 1300 x 10(4)/ml) after discontinuation of mepitiostane and administration of human chorionic gonadotropin (HCG). This clinical study suggests that some anabolic steroids play a role in uremic hypogonadism; thus mepitiostane or its analogues should be carefully prescribed for young male patients.


Donaldson IA, Hart IC, Heitzman RJ. Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol. Res Vet Sci 1981;30(1):7-13. Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with ... - PubMed - NCBI

The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.

Perhaps I'm misinterpreting this post but I don't think 19nors raise prolactin levels as commonly bro-thesized. I was responding to IronWill when he asked what you thought was broscience.

 

[Michael Scally MD]

Perhaps I'm misinterpreting this post but I don't think 19nors raise prolactin levels as commonly bro-thesized. I was responding to IronWill when he asked what you thought was broscience.

TY

 

[Docd187123]

If I understood the mechanism behind the lethargy caused by the Prami, I might be able to counteract that side effect with something.

Thanks Doc for your input/references. Question. Do you have such posts by people like Michael Scally bookmarked on your computer or are you searching on Meso in a certain way. My personal search results on this sight always come back screwy. One comment I noticed in that research was that the estrogen stemming from the exogenous testosterone caused feedback to increase the production of Prolactin. That is sensible.

I have some pages bookmarked, some I just remember how to find, and others I use google for. I can never get the Meso search feature to work right for me.

 

[RaveHead]

I have some pages bookmarked, some I just remember how to find, and others I use google for. I can never get the Meso search feature to work right for me.

So instead of using the Meso search function, you simply type into Google the same search terms and tack on Meso at the end?

 

[Docd187123]

So instead of using the Meso search function, you simply type into Google the same search terms and tack on Meso at the end?

Basically. If I want a particular member's post I'll add that members name.

 

[Throwback]

You need to control estrogen. Forget about prami and caber for now. Worry about your AI, E2, and bloodwork.

This....manage estrogen. Problem solved. No need for pramipexole.

 

[RaveHead]

This....manage estrogen. Problem solved. No need for pramipexole.

Yes. Agreed. I am just also looking into "biohacking" and neuroendocrine balancing throughout my normal AAS courses. I love looking for ways to optimize everything I can while minimizing negative sides.