Why do some people suggest am AI during a cycle?

[Ryno1980]

Sensitivity can be from anything really. If it hasn't grown when it normally would have, then you know the nolva is working for you.

OK so I shouldn't worry that it's noticeably sensitive when I touch it? I only ask because this is the first cycle since getting this lump... I just don't want to make it worse... I would think the nolva and 1mg adex e4d would keep it from doing so

 

[ChestRockwell]

You want to monitor actual growth (fibrosis) however sensitivity will come and go (even for those who may not have any actual gland tissue growth).

I've actually had "sensitivity" after eating certain types of meals before, oddly enough. So yeah, don't overly stress to the point where it becomes a problem (e.g. keep touching and squeezing until it does become a problem).

 

[Docd187123]

OK so I shouldn't worry that it's noticeably sensitive when I touch it? I only ask because this is the first cycle since getting this lump... I just don't want to make it worse... I would think the nolva and 1mg adex e4d would keep it from doing so

Just what Chest said brother.

 

[combover]

Does pubescenct gyno indicate a propensity to develop further when using aas?

 

[Just Fish]

OK so I shouldn't worry that it's noticeably sensitive when I touch it? I only ask because this is the first cycle since getting this lump... I just don't want to make it worse... I would think the nolva and 1mg adex e4d would keep it from doing so

Did you get your prolactin and progesterone tested? 19 nor's in the amount your taking could cause problems such as gyno. If the problem is the deca and npp something like caber will fix your issue. The only way to really know is with blood work though

 

[Qbanfreak90]

You need blood work in order to know exactly what's going on inside you can't go by feel all the time.


Sent from my iPhone using Tapatalk

 

[Docd187123]

Did you get your prolactin

Why should he? Tren and deca dot raise prolactin.

19 nor's in the amount your taking could cause problems such as gyno.

Prolactin doesn't cause gyno prolactin doesn't increase bc of 19nor use.

If the problem is the deca and npp something like caber will fix your issue. The only way to really know is with blood work though

No, caber only treats elevated prolactin but not gyno

 

[Just Fish]

High prolactin levels and prolactinomas

 

[Just Fish]

Hyperprolactinaemia - Wikipedia

 

[Just Fish]

Prolactin & Anabolic Steroids - Steroidal.com

 

[Just Fish]

^^^^^^^^^^^^^^^^^^^^^^^^

Why should he? Tren and deca dot raise prolactin.



Prolactin doesn't cause gyno prolactin doesn't increase bc of 19nor use.



No, caber only treats elevated prolactin but not gyno

Can you explain to me what causes "deca-dick"?

 

[Just Fish]

Why should he? Tren and deca dot raise prolactin.



Prolactin doesn't cause gyno prolactin doesn't increase bc of 19nor use.



No, caber only treats elevated prolactin but not gyno

Read the three articles in the links I sent you

 

[Docd187123]

^^^^^^^^^^^^^^^^^^^^^^^^


Can you explain to me what causes "deca-dick"?

What causes testosterone dick? What causes equipoise dick? What causes masteron dick?

I ask bc there are plenty of people who complain about the same issue with other compounds. You're saying ALL compounds can raise prolactin or that all "dick" issues are prolactin related????

Read the three articles in the links I sent you

I did but I also LOL'ed at you using Wikipedia and Steroidal.com as legitimate references. Your Uptodate reference was a good one but unfortunately did nothing to help your position. Would you care to try again, this time using an actual legitimate reference that supports your opinion?

 

[Docd187123]

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.

 

[Docd187123]

The answers to your questions are fairly obvious. If the compound aromatizes, interacts with the estradiol receptor, then there will be an effect on prolactin secretion. The same effects would be expected in a "healthy" person taking AAS. The abstracts above address the questions directly. The estradiol produced from testosterone in TRT will "overpower" the negative dopamine agonist effect of cabergoline, therefore the use of an aromatization inhibitor.

An overview of the regulation of prolactin secretion. Prolactin secretion is paced by a light-entrained circadian rhythm, which is modified by environmental input, with the internal milieu and reproductive stimuli affecting the inhibitory or stimulatory elements of the hypothalamic regulatory circuit. The final common pathways of the central stimulatory and inhibitory control of prolactin secretion are the neuroendocrine neurons producing prolactin inhibiting factors (PIF), such as dopamine (DA), somatostatin (SST), and gamma-aminobutyric acid (GABA), or prolactin releasing factors (PRF), such as thyrotropin releasing hormone (TRH), oxytocin (OT), and neurotensin (NT).

PIF and PRF from the neuroendocrine neurons can be released either at the median eminence into the long portal veins or at the neurointermediate lobe, which is connected to the anterior lobe of the pituitary gland by the short portal vessels. Thus lactotrophs are regulated by blood-borne agents of central nervous system or pituitary origin (alpha-melanocyte stimulating hormone) delivered to the anterior lobe by the long or short portal veins. Lactotrophs are also influenced by PRF and PIF released from neighboring cells (paracrine regulation) or from the lactotrophs themselves (autocrine regulation).

View attachment 7320

Direct effects of neurotransmitters, neuromodulators, and peripheral hormones on the activity of tuberoinfundibular dopaminergic system (TIDA). The inhibitory agents (left) will promote an increase of prolactin secretion as a result of diminishing TIDA activity. On the other hand, the stimulatory neurotransmitters and progesterone (right) will tend to decrease prolactin secretion as a result of increasing output of TIDA neurons.

It should be noted, however, that many of these agents have multiple levels of action, often with opposing biological effect. Therefore, in some cases (*), effects on PRF and/or directly at the lactotrophs will prevail over the influence on TIDA activity.

Key: 5-HT, serotonin; NE, norepinephrine; HA, histamine; EOP, endogenous opioid peptides (endorphin, enkephalin, dynorphin, nociceptin/orphanin); GAL, galanin; SST, somatostatin; CCK8, cholecystokinin-8; GABA, gamma-aminobutyric acid; NO, nitric oxide; ACh, acetylcholine; TRH, thyrotropin releasing hormone; OT, oxytocin; VP, vasopressin; VIP, vasoactive intestinal polypeptide; PACAP, pituitary adenylate cyclase-activating peptide; ANG II, angiotensin II; NT, neurotensin; NPY, neuropeptide Y; CT, calcitonin; BOM, bombesin-like peptides (gastrin-releasing peptide, neuromedin B, neuromedin C); ANP, atrial natriuretic peptides.

View attachment 7321

 

[Just Fish]

What causes testosterone dick? What causes equipoise dick? What causes masteron dick?

I ask bc there are plenty of people who complain about the same issue with other compounds. You're saying ALL compounds can raise prolactin or that all "dick" issues are prolactin related????



I did but I also LOL'ed at you using Wikipedia and Steroidal.com as legitimate references. Your Uptodate reference was a good one but unfortunately did nothing to help your position. Would you care to try again, this time using an actual legitimate reference that supports your opinion?

I said 19 nor's raise prolactin. I didn't say anything about other compounds.
WHAT CAUSES DECA-DICK?

 

[Just Fish]

Thats a rhetorical question by the way. Figured you might learn something from it

 

[Jeremiahflex]

The only issue I've ever had with nandrolone is the inability to bust a nut in a timely manner, never heard of "testosterone dick" though. would be nice to know the triggers of all these symptoms.

 

[ChestRockwell]

The overly simplified answer would be the body's A:E (androgen:estrogen) ratio being in an individual's sweet spot.

This is not unique to any one compound and A:E ratios being out of whack is largely responsible for most "estrogen related" problems in the hormone world.

 

[Just Fish]

Prolactin doesn't cause gyno prolactin doesn't increase bc of 19nor use.

High prolactin levels and prolactinomas