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Fina users read this ( prolactin )


New member
Feb 4, 2003
Fina users,, read this on prolactin
Here is an avenue that has not been explored in this thread: The potential relationship between trenbolone, thyrotropin-releasing hormone (TRH) and prolactin. TRH stimulates the synthesis and release of thyrotropin (thyroid stimulating hormone) from the pituitary. Thyrotropin in turn stimulates the release of the thyroid hormones. A negative feedback loop exists whereby low levels of T4 stimulate the release of TRH (1).

It has been established that in humans TRH is also capable of stimulating the release of prolactin (2). In hypothyroid patients there is often an elevation of TRH and prolactin due to diminished levels of T4. (3) Galactorrhea often presents as a symptom of hypothyroidism.

In sheep, administration of trenbolone acetate results in 45% decrease in thyroxine levels (4). This should exert a stimulatory effect on TRH. ( Interestingly, the same study shows that unlike in humans prolactin levels in the sheep remained unchanged. This is due to the fact that in sheep, unlike in humans, TRH and prolactin are secreted independently of each other (5).)

If it assumed that trenbolone acetate also lowers thyroxine levels in humans, the resulting rise in TRH would stimulate prolactin release, leading to galactorrhea and gynecomastia.

Due to the lack of human studies involving tren, we are all forced to speculate, and try to extrapolate from animal studies.

(1)Endocrinology 1999 Jan;140(1):43-9

Feedback regulation of thyrotropin-releasing hormone gene expression by thyroid hormone in the caudal raphe nuclei in rats.

Yang H, Yuan P, Wu V, Tache Y.
Digestive Diseases Research Center, West Los Angeles VA Medical Center, Department of Medicine and Brain Research Institute, UCLA, California 90073, USA. [email protected]

(2)Goodman and Gilman's The Pharmacological Basis of Therapeutics 8th ed. pp.1345-1346

(3) : Endocr J 1997 Feb;44(1):89-94

Incidence of hyperprolactinemia in patients with Hashimoto's thyroiditis.
Notsu K, Ito Y, Furuya H, Ohguni S, Kato Y.
Department of Medicine, Shimane Prefectural Central Hospital, Izumo, Japan.

(4)Res Vet Sci 1981 Jan;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 oestradiol.

Donaldson IA, Hart IC, Heitzman RJ.

(5) Endocrinol 1988 Apr;117(1):115-22

Release of prolactin is independent of the secretion of thyrotrophin-releasing hormone into hypophysial portal blood of sheep.

Thomas GB, Cummins JT, Yao B, Gordon K, Clarke IJ.
Medical Research Centre, Prince Henry's Hospital, Melbourne, Australia.

Yes, finally!!! you hit the nail right on the head.

Fina is a VERY POWERFUL anti-glucocorticoid, so what
exactly does it do to reduce endogeneous cortisone

There is only ONE mechanism:

A reduction in the TOTAL Free T4 and T3 levels within the

T3 is HIGHLY catabolic to muscle, therefore by reducing it by(
take 45% as shown by Nandi as an example), you are
exerting a ridiculously high protein-sparing effect.

YES, thats right, Fina is not THAT anabolic IN VIVO, it is
far, and I do mean FAR more of an ANTI-CATABOLIC
AAS than anything else.

Ok, now lets back-track to the problem at hand.

TSH has been reduced by the trenbolone, which in
turns signals the thyroid to reduce endogeneously
produced levels of T3 and T4.

This reduction(As Nandi mentioned) causes a VERY
sharp drop in free T3 levels because of the reduction
in both the endogeneously produced T4 and T3.
(Remember that 80% of the free T3 is produced from
the metabolically inactive T4)

These dimished levels of T3,T4 cause Thyrotropin Releasing
Hormone(TRH) to become OVER-STIMULATED.

In essence, this is your bodies feed-back loop to reduced
thyroid hormones, due to a GLUCO-CORTICOID suppresive
effect. This is however NOT like hypothyroidic patients
who have a naturally defective(or damaged) thyroid.

When TRH becomes over-stimulated the net effect is
a VERY sharp increase in prolactin levels.

Critical here.....


Now, herein lies the problem. Everybody is bio-chemically
different, therefore the TRH increase is EXTREMELY

While someone will stimulate TRH say X% and ultimately
cause a rise in prolactin of say Y% with a daily
dosage of 50mg ED of Fina, another person will
cause a 2X% rise in TRH and 2Y+% rise in prolactin
which will invariably lead to gyno.

This is just genetics. Nothing can be done about this.

However, there are ways to combat prolactin-elevations:

This btw, HAS TO BE EXACT. If you over-dose you cause
a progestenic shift due to severely inhibited prolactin levels,
or if you under-dose you run the risk of getting prolactin
induced gyno.

As a note: PROGESTERONE does NOT, I repeat NOT come into
play with Fina at all. It only becomes into play when you're
trying to inhibit prolactin synthetically.

The only thing that can combat Fina-induced Gyno is:

1. 2.5mgs Bromocriptine broken down to 1.25mgs 2X/day
AM and PM.

Thats it.

No Vitex/Nolva/Clomid/Arimidex or whatever. They don't
work for Fina.

Those would work well with Deca. Winny would be the only help I would see with A-drol. That is one crazy substance
Part 2
I got more info regarding prolactin. This one I got from T-mag.com

Lost: One Sex Drive. Answers to the name of "Woody"

Q: Is there anything a person can do to get his sex drive back after a cycle? Even with Clomid this seems to take a while.

A: If you simply want to increase the urge to have sex, then you can go with clomiphene along with bromocriptine or something like vitex which is found in Biotest's M. The reason is simply because these substances are dopamine agonists which can lower the production of prolactin (prolactin decrease sex drive and is often elevated after a cycle of Testosterone and other androgens). When prolactin is decreased, sex drive can increase rather dramatically. (There was even a case in the UK where a man sued the makers of bromocriptine since it gave him an uncontrollable sex drive.)

So why should we care about inhibiting prolactin secretion? Let me explain. First off, estrogen and prolactin are related in terms of their release. In other words, when estrogen rises, so does prolactin. Who gives a rat's ass? You should for a few reasons, one being that it decreases LH and Testosterone. There's also a good amount of evidence suggesting prolactin is partially responsible for the degree of sensitivity in terms of gonadal steroid feedback (negative feedback) and may even regulate the sensitivity of the gonads to stimulation by LH.

In one study researchers took eleven normal men and studied them both during hyperprolactinemia and hypoprolactinemia. What they found was that LH rose in a state of hypoprolactinemia. However, in men, it's been shown time and time again that elevated prolactin leads to decreased gonadotropin levels (LH).

Furthermore, in a study with men who had elevated prolactin levels, they decided to measure the effect of hCG (acts like LH) administration on Testosterone production. What they found was that in hyperprolactinemic men, their response to hCG administration (measured in terms of Testosterone levels) was significantly lower than that of men with normal prolactin levels. When they treated the individuals with hyperprolactinemia and reduced prolactin levels, they found the increase in Testosterone after hCG administration was much higher.

So you think your prolactin levels will never rise? Think again. If your Testosterone rises (and thus estrogen rises via conversion by the aromatase enzyme), your prolactin will rise as well. Furthermore, prolactin has been shown to rise in times of stress. As we know, the combination of everyday life and bodybuilding can produce a large amount of stress. On a side note, this once again confirms to me that methandrostenolone (D-bol) increases dopamine levels and thus increases sex drive.
Let me see if I understand. Knowing prolactin is the 'master' female hormone; you report it rises in accordance with rises in estrogen levels. Wouldnt feedback cause the prolactin to LOWER (as the body recognizes the incresed level of estrogen and lowres the master hormone as not to continue to produce more)
in the same fashon that raised test leves will induce the feedback system to lower release of FHS and LH? I could see prolactin levels rising and causing a rise in estrogen (how it would occur endogeniously and naturally) but if the rise in estrogen came first from an exogenious source, Id figure prolactin would lower, at least temporarily.
And progesterone is also a female hormone-why doesnt prolactin increase also contribute to raised progesterone?
And one thing as was stated fina is not a good anabolic, just a great anti-corticol. As this may be true; but fina has a Threraputic Index of 500/500 with pure testosterone the measuring stick at 100/100. Thats ratio of anabolic to androgenic properties. So in other words, mg for mg, fina is 5x as anabolic, AND androgenic, as test. Thats not bad at all!
Im not questioning any of your material - actually I found it so fascinating and educational that I printed it! But I want to understand what I THINK (I may be wrong and that why Im asking) is correct and how it related to some of the info in the studies. Thanks for a great post.
there is a post on AF about using B6 as a way to combat prolactin. Apparently there have been some studies done where 3 doses of b6 daily completely stopped female lactation by decreasing prolactin. I'm very sensitive to tren gyno, so I'm going to try the B6 when I start my cycle. (I have bromocriptine on hand in case the B6 doesn't work)

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