questions about tren cycle

[Docd187]

I agree estrogen must be controlled, but not because of prolactin. Tren does not aromatize and controlling estrogen does not eliminate high prolactin levels, when running it. Likewise, running test alone does not create prolactin issues, even thou it significantly increases estro without an AI.

Estrogen from my understanding of the reading can LEAD to prolactin issues and compounds prolactin problems from compounds such as tren. You are right controlling estrogen does not totally eliminate high prolactin levels but it is extremely important nonetheless. Yes dopamine agonists are your best bet to control serum prolactin levels once its become an issue, but you can possibly avoid the issue altogether by regulating estrogen from the very beginning.

Granted its on mice but:

There is an increasing body of evidence implicating estradiol in the regulation of prolactin synthesis and secretion.Recent work from our laboratory demonstrated that treatment of rats with estradiol specifically increased the incorporation of pre- cursors into prolactin(1)and led to the accumulation of pre- prolactin mRNA in the pituitary(2).The results indicate that estradiol stimulates prolactin synthesis through direct action on the pituitary.

Estrogen control provides a well-studied positive control over prolactin synthesis and secretion. An example of this is the increasing blood concentrations of estrogen during late pregnancy appear responsible for the elevated levels of prolactin that are necessary to prepare the mammary gland for lactation at the end of gestation.

Prolactin

http://www.pnas.org/content/75/12/5946.full.pdf

and that blocking the effects of estrogen, or increasing T + dihydrotestosterone levels, is central to ameliorating the problem.

prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels (see Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607)

 

[Docd187]

And my previous post #19 left out some quotes when I quoted it lol more geared towards progesterone but still relevant since tren is the topic so I'm editing it and hopefully everything makes it in this time

 

[2rude4u]

Estrogen from my understanding of the reading can LEAD to prolactin issues and compounds prolactin problems from compounds such as tren. You are right controlling estrogen does not totally eliminate high prolactin levels but it is extremely important nonetheless. Yes dopamine agonists are your best bet to control serum prolactin levels once its become an issue, but you can possibly avoid the issue altogether by regulating estrogen from the very beginning.

Granted its on mice but:




Prolactin

http://www.pnas.org/content/75/12/5946.full.pdf

Mice are not men so here's a simpler way for me to explain what I'm saying to you with two questions.

1. Have you ever known someone to run test only and develop prolactin issues?

I'm sure it can happen, but in a very, very small amount of cases.

2. Have you ever know someone to run test and tren with an Aromatase inhibitor (AI), but still develop Prolactin issues?

I know for a fact you can't say no because many guys with that exact situation have posted here numerous times about it. Even thou they ran an Aromatase inhibitor (AI) and kept estro in check they still developed prolactin issues. So what does this tell you?

 

[Docd187]

Mice are not men true but rat mammary glands share so many similarities with those of humans that researchers themselves often have hard times distinguishing tissues of the two along with the fact that rat mammary glands are the foremost animal model for studies done on human breast tissue because of the extreme similarities in structure, form and function. To dismiss them simply because they are mice is just as rash as IF I had said estrogen was the SOLE factor to consider in prolactin issues.

Number one tells me that you've acknowledged estrogen plays a role in prolactin development and number two tells me that there are factors besides estrogen in the production and control of prolactin. Both of which I've already said. I've never said estrogen control is the sole remedy, but that it is a very crucial step towards it. Just because someone ran an Aromatase inhibitor (AI) on cycle does not mean they controlled their Estrogen. You would have to have bloodwork for each and every anecdotal case since you can't be sure the Aromatase inhibitor (AI) was not bunk/under dosed, the dosing protocol followed was sufficient to control a certain individual's estrogen levels and their pre-disposition towards aromatization, and that they had no drug interactions that limited the efficacy of the Aromatase inhibitor (AI) (such as is the case with anastrozole and tamoxifen, I've seen numerous ppl here take both at the same time).

I agree with you dopamine agonists are the best way to control prolactin release and problems. But the same way you argue "someone who ran test and tren and an Aromatase inhibitor (AI) to control estrogen had issues with prolactin" makes possible the argument what about "the ppl who run test and tren and Aromatase inhibitor (AI) and DO NOT have prolactin issues WITHOUT dopamine agonists"?? At the end of all this I'm not saying to RELY SOLELY on estrogenic control of prolactin secretion. To do so would be foolish. I'd always recommend having caber, prami, bromo, or dost on hand to treat possible issues. I am arguing that you MAY NOT need them so long as estrogen is truly under control.

One example of a prolactin-stimulating factor for which a role has been identified is estrogen

There is an increasing body of evidence implicating estradiol in the regulation of prolactin synthesis and secretion.Recent work from our laboratory demonstrated that treatment of rats with estradiol specifically increased the incorporation of pre- cursors into prolactin(1)and led to the accumulation of pre- prolactin mRNA in the pituitary(2).The results indicate that estradiol stimulates prolactin synthesis through direct action on the pituitary.

The effect of estrogen on the dopaminergic control of PRL secretion was investigated. Treatment of groups with estradiol benzoate (25 microgram/kg, sc) daily for 5 days resulted in a marked elevation of the serum PRL concentration.

Abstract

Plasma prolactin as determined by radioimmunoassay was barely detectable in 21-day-old fetuses and on the day of birth (day 0). It had declined by days 3***8211;6 and then rose gradually to attain adult levels at day 35. To further evaluate (he development of the prolactin control system, the ability of estrogen to elicit prolactin release was studied at various ages by injecting different doses of estradiol benzoate (Eb) SC once daily lor 2 days and measuring plasma prolactin 24 hr after the last injection. At 11 days of age, there was no significant increase in prolactin with any of the doses of Eb used (0.05***8211;0.4 µg/100 g body wt). In 27-day-old rats, the 0.4 µg dose induced a dramatic rise in plasma prolactin and the 0.05, 0.10 and 0.2 µg dose induced much smaller but significant increases in prolactin. By 37 days, the 0.2 µg dose became highly effective and the 0.4 µg dose induced an even larger increase. The response of adult females to this dose was significantly less than that observed in 37-day-old animals. In a subsequent experiment, the time of first response to estrogen was determined more exactly t o be 24 days of age. The maturation of the dopaminergic inhibitory control of prolactin release was studied by injecting the dopamine (DA) receptor blocker, Pimozide (0.63 mg/kg, SC), at different ages. The drug significantly elevated plasma prolactin as early as the third day of life and the magnitude of this response then increased progressively up to 35 days of age. It is suggested that plasma prolactin levels during development in the female rat depend on the balance between the stimulatory effect of estrogen on prolactin release and the inhibitory control exerted by the hypothalamic dopaminergic system. (Endocrinology 95: 149.9,1974)

The data presented here demonstrate that chronic administration of relatively small amounts of EE to postmenopausal and ovariectomized women induced an augmented pituitary PRL secretion that was accompanied by a pattern of increased fluctuation (Table I and Fig. 1). This action of estrogen is prompt, with serum PRL concentrations more than doubling in 1 wk and reaching a peak by the 3rd wk to levels of more than 3 times the initial concentrations (Fig. 2). It is evident that EE exerted an opposite action between the augmented PRL secretion and the suppressed gonado- tropin release. These data represent the first clear dem- onstration of the enhancement of estrogen on pituitary PRL-release in humans. In normal male subjects, Frantz, Kleinberg, and Noel have recently shown that estrogen treatment for 1 wk induced a clear rise in PRL levels in subjects. In patients with prostatic carcinoma receiving chronic estrogen therapy, the mean PRL level was found to be twice the normal male values (20.7 vs. 9.2 ng/ml) (4).

From the experimental data obtained in rats, estrogen appears to cause the enhanced PRL release by exerting adualactionviahypothalamicsuppressionofthePRL- inhibiting factor and direct stimulation of pituitary lac- totrophs. (1-3). In humans, substantial evidence is now available to indicate a temporal relationship between pituitary PRL secretion and estrogen levels; a rise in PRL concentration parallel with the increase in circulating estrogen was found. These collective observations together with our present finding suggest that estrogen exerts a positive feedback effect on pituitary PRL secretion but does not provide evidence favoring primary hypothalamic vs. pituitary or a com- bined site of action. Participation of other hormonal eventsintheaugmentationofPRLrelease,especially during pregnancy, should also be considered.

 

[2rude4u]

Mice are not men true but rat mammary glands share so many similarities with those of humans that researchers themselves often have hard times distinguishing tissues of the two along with the fact that rat mammary glands are the foremost animal model for studies done on human breast tissue because of the extreme similarities in structure, form and function. To dismiss them simply because they are mice is just as rash as IF I had said estrogen was the SOLE factor to consider in prolactin issues.

Number one tells me that you've acknowledged estrogen plays a role in prolactin development and number two tells me that there are factors besides estrogen in the production and control of prolactin. Both of which I've already said. I've never said estrogen control is the sole remedy, but that it is a very crucial step towards it. Just because someone ran an Aromatase inhibitor (AI) on cycle does not mean they controlled their Estrogen. You would have to have bloodwork for each and every anecdotal case since you can't be sure the Aromatase inhibitor (AI) was not bunk/under dosed, the dosing protocol followed was sufficient to control a certain individual's estrogen levels and their pre-disposition towards aromatization, and that they had no drug interactions that limited the efficacy of the Aromatase inhibitor (AI) (such as is the case with anastrozole and tamoxifen, I've seen numerous ppl here take both at the same time).

I agree with you dopamine agonists are the best way to control prolactin release and problems. But the same way you argue "someone who ran test and tren and an Aromatase inhibitor (AI) to control estrogen had issues with prolactin" makes possible the argument what about "the ppl who run test and tren and Aromatase inhibitor (AI) and DO NOT have prolactin issues WITHOUT dopamine agonists"?? At the end of all this I'm not saying to RELY SOLELY on estrogenic control of prolactin secretion. To do so would be foolish. I'd always recommend having caber, prami, bromo, or dost on hand to treat possible issues. I am arguing that you MAY NOT need them so long as estrogen is truly under control.

As I said previously... I agree with you that estro control is important. As much as I enjoy a good discussion we have gotten so far off track I nearly forgot the original question, which was:

is the keep your E low and your prolactin will stay under control, is that a myth or is it real?

To which I replied Myth and IMO is the correct answer. Do you not agree?