MESO-Rx

Anabolic Steroids

Deca Dick.

SJB78 said:
So I've been thinking and I think most of you guys are right in regards to dumping the deca. So I've decided that it's time to say goodbye to the deca and switching to masteron for the remainder of my cycle which is 8 weeks. Since deca is a long ester I will hit my dr up for some viagara as I expect my ed will continue until the steroid has cleared from my system. Their have been some good lessons learnt though and they are:
A) My deca is good shit and legit
B) In future I will run equipoise instead of deca
C)No steroid is worth loosing the use of your dick
D)Chicks love guys who have a great physique however if you can't perform in bed she will leave you in a heartbeat for a skinny 60kg guy with hard cock
E)Getting off drugs and training will help you get the girl you always wanted.
Thanks for the input fellas. I'll let you know how it all goes......
Click to expand...
I've read it's possible 19nors can influence prolactin levels which is the reason why people get 'deca dick'
 
SJB78 said:
So three years ago was the last time that I ever had sex as I relapsed on drugs and was too busy being a junkie rather than looking good and getting pussy. Over a year ago I got clean, started training again, started aas again and now I'm looking pretty fucken good. So 2 weeks ago I was with the girl of my dreams who I think is hot as fuck and picked up on body language and some pheromones and realized she wanted to get down to business. It started off all passionate and shit like the movies then bam! Deca dick. I couldn't get rock hard like I used too. WTF I thought. 3 years and then this. So I'm 8 weeks into a test e, deca and dbol stack (finished dbol at week 6) and it's going great. I'm also on arimidex at 1mg eod. Obviously without bloods it's hard to say whether it's directly related to the deca (500mg/pw) or estrogen however my question is will Viagara help my situation until I get bloods?
If you got this far thanks for hanging in there.
Click to expand...

I know your struggle, it' embarrassing :(
 
tattedlegend said:
I've read it's possible 19nors can influence prolactin levels which is the reason why people get 'deca dick'
Click to expand...

Absolutely, prolactin is the hormone you release after the big O. Which is the reason you can't get hard again for however long.
 
I still dont get the deca dick thing. Granted Im using it for the first time and only 400mg/wk, but 8 weeks in Im having some of the best boners of my life. Im talking high school, scrambled spice channel, I just saw a nipple boners. Lately I dont even want to "dive right in" I just like to stand there (like cpt. morgan) so me and a female can admire it.
 
mafaon said:
Just get the Viagra dude. It will put your mind at ease and you'll have the hardest wood imaginable. In fact I think anyone doing a cycle should have Viagra on them as a backup for situations like this.
Click to expand...

Use Melanotan II. Get good wood and a tan. Win win
 
tattedlegend said:
True, but is there evidence showing that 19nors do not effect prolactin as well. To my understanding there is no research or evidence proving and supporting either claim?
Click to expand...

The burden of proof is on the ones making the claim which happens to be the ppl saying 19nors do affect prolactin.

Here are some studies that might interest you:

Anabolic steroid-associated hypogonadism in male hemodialysis patients.
Maeda Y, et al. Clin Nephrol. 1989.
Show full citation
Abstract
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.

PMID
2805460 [PubMed - indexed for MEDLINE]

Granted this one is on sheep but tren and humans hasn't been extensively studied....

Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.
Donaldson IA, et al. Res Vet Sci. 1981.
Show full citation
Abstract
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.

PMID
7017853 [PubMed - indexed for MEDLINE]

Sodi R, Fikri R, Diver M, Ranganath L, Vora J. testosteronereplacement-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.
 
guys are going way too high on deca nowadays, 300mg/wk is all you need, 500/wk and say goodbye to your dick for half the cycle
 
Docd187123 said:
The burden of proof is on the ones making the claim which happens to be the ppl saying 19nors do affect prolactin.

Here are some studies that might interest you:

Anabolic steroid-associated hypogonadism in male hemodialysis patients.
Maeda Y, et al. Clin Nephrol. 1989.
Show full citation
Abstract
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.

PMID
2805460 [PubMed - indexed for MEDLINE]

Granted this one is on sheep but tren and humans hasn't been extensively studied....

Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol.
Donaldson IA, et al. Res Vet Sci. 1981.
Show full citation
Abstract
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.

PMID
7017853 [PubMed - indexed for MEDLINE]

Sodi R, Fikri R, Diver M, Ranganath L, Vora J. testosteronereplacement-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.
Click to expand...
Thanks for posting these doc they are an interesting read.
 
I'm drawing blood in 1 week and half after 6-7 weeks of deca... Need to check out the exact week I'm in. Anyway I have prolactin and progesterone baseline before starting deca.

We will have an answer to this damn bro science that it's floating around for ages :D
 
Just remember that estradiol can cause raised prolactin levels. I don't think it matters if that estradiol is coming from testosterone or nandrolone.
 
Sampei said:
I'm drawing blood in 1 week and half after 6-7 weeks of deca... Need to check out the exact week I'm in. Anyway I have prolactin and progesterone baseline before starting deca.

We will have an answer to this damn bro science that it's floating around for ages :D
Click to expand...
This will be good.
 
jaymaximus said:
I still dont get the deca dick thing. Granted Im using it for the first time and only 400mg/wk, but 8 weeks in Im having some of the best boners of my life. Im talking high school, scrambled spice channel, I just saw a nipple boners. Lately I dont even want to "dive right in" I just like to stand there (like cpt. morgan) so me and a female can admire it.
Click to expand...
come back after your cycle and let us know how things are going
 
Sampei said:
I'm drawing blood in 1 week and half after 6-7 weeks of deca... Need to check out the exact week I'm in. Anyway I have prolactin and progesterone baseline before starting deca.

We will have an answer to this damn bro science that it's floating around for ages :D
Click to expand...

Nice. Please Keep us updated.
 
SJB78 said:
So three years ago was the last time that I ever had sex as I relapsed on drugs and was too busy being a junkie rather than looking good and getting pussy. Over a year ago I got clean, started training again, started aas again and now I'm looking pretty fucken good. So 2 weeks ago I was with the girl of my dreams who I think is hot as fuck and picked up on body language and some pheromones and realized she wanted to get down to business. It started off all passionate and shit like the movies then bam! Deca dick. I couldn't get rock hard like I used too. WTF I thought. 3 years and then this. So I'm 8 weeks into a test e, deca and dbol stack (finished dbol at week 6) and it's going great. I'm also on arimidex at 1mg eod. Obviously without bloods it's hard to say whether it's directly related to the deca (500mg/pw) or estrogen however my question is will Viagara help my situation until I get bloods?
If you got this far thanks for hanging in there.
Click to expand...
you have to run test with the deca twice as much as deca
 
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