Yo Fina users: read this on Prolactin

[Drveejay11]

(GREAT post, unsure who the Original author was)

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. hoyang@ucla.edu

(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
levels?

There is only ONE mechanism:

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

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.....

I.E. YOU BEGIN TO LACTATE!!!!!

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

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. Winstrol (winny) would be the only help I would see with A-drol. That is one crazy substance.

 

[hhajdo]

LOL, not this again.
If you read the post you can see that it's based on speculation.
It's beleived that tren & deca are PR agonists, which is one of the reasons they can contribute to gyno.

The author of that post is nandi.



Prolactin increase is caused by elevated estrogen.

Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72

Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation.

Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F.

A case of a patient with hypopituitarism due to a disturbance of hypothalamo-pituitary regulation is presented, who developed high-grade hyperprolactinaemia after the initiation of substitutive therapy with testosterone esthers.The increase in serum Prl was strictly related to testosterone aromatization to oestradiol, since anti-oestrogen compounds were effective in reducing (clomiphene) or abolishing (tamoxifen) the enhanced Prl secretion. The oestrogen effect in raising Prl release was not attributable to a reduction in the dopamine inhibition of Prl-secreting cells, as the dopamine-antagonist domperidone failed to increase Prl serum levels in the same patient. This suggests that, in man, the oestrogen effect in enhancing Prl release is mainly enacted directly on the pituitary lactotrophs rather than exerted through a reduction in the hypothalamic dopamine activity.


----------------------------------------


Clin Endocrinol (Oxf) 1982 Nov;17(5):495-9 Related Articles, Links


Hydrotestolactone lowers serum oestradiol and PRL levels in normal men: evidence of a role of oestradiol in prl secretion.

D'Agata R, Aliffi A, Maugeri G, Mongioi A, Vicari E, Gulizia S, Polosa P.

The effect on serum PRL levels of lowering serum oestradiol (E2) concentration by short-term administration of an aromatase activity inhibitor, hydrotestolactone (HT), was studied in six healthy male subjects. After HT administration serum E2 levels decreased from 68 +/- 5.8 to 26 +/- 2.5 pmol/l (mean +/- SE, P less than 0.05). These E2 changes were accompanied by a significant decrease in mean 2-h PRL levels from 11.2 +/- 2.1 to 6.5 +/- 1.6 ng/ml mean +/- SE, P less than 0.05). The evaluation of individual percentage change from basal concentrations showed a varying decrease in all subjects. These findings suggest that under physiological conditions E2 may be one of the factors which control blood PRL concentrations in men


--------------------------------------


Life Sci 2001 Mar 2;68(15):1769-74 Related Articles, Links


Effect of androgenic anabolic steroids on sperm quality and serum hormone levels in adult male bodybuilders.

Torres-Calleja J, Gonzalez-Unzaga M, DeCelis-Carrillo R, Calzada-Sanchez L, Pedron N.

Unidad de Investigacion Medica en Biologia de la Reproduccion, Instituto Mexicano del Seguro Social, Mexico, DF.

The purpose of this study was to assess the influence of the administration of high doses of androgenic anabolic steroids (AAS) on endocrine and semen parameters. Thirty volunteering bodybuilders were studied (ages ranging between 26.6 +/- 4.1 years). A history of anabolic steroid administration was recorded for fifteen subjects, and results of semen analysis and endocrine parameters were compared with data from fifteen bodybuilders not using steroids. In those subjects using AAS, eight had sperm counts under the lower normal limit (20 x 10(6) sperm/ml), three had azoospermia, two polyzoospermia, and two had normal sperm counts. The percentage of morphologically normal sperm was significantly reduced, only 17.7% had normal spermatozoa. In the control group, only one subject had oligozoospermia. The hormonal parameters revealed reduced FSH (1.5 +/- 3.2 vs 5.0 +/- 1.6, p < 0.001) and PRL (5.1 +/- 4.9 vs 9.2 +/- 4.4, p < 0.01) levels. LH, T, E2 and DHEA levels did not vary.


-----------------------------------


Chronic use of bromo can cause hypoprolactinemia which can hinder HPTA recovery:


Fertil Steril 1991 Feb;55(2):355-7

Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.

Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.

Department of Medicine, Shimane Medical University, Japan.

To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (hCG) stimulation were measured every 2 weeks.Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo


Some OTC supplements like St. John's wort may lower prolactin


Pharmacopsychiatry 2001 Jul;34 Suppl 1:S29-37 Related Articles, Links


Researching the antidepressant actions of Hypericum perforatum (St. John's wort) in animals and man.

Franklin M, Cowen PJ.

University of Oxford Department of Psychiatry, Warneford Hospital, UK.

We have studied the effect of acute and sub-chronic treatments of a formulation of a methanolic extract of hypericum perforatum (HP, also known as St John's wort) on plasma hormones and brain neurotransmitters in healthy human volunteers and rats. Also studied were the effects of equivalent acute doses of two constituents of HP (with respect to LI 160 extract), hypericin and hyperforin in rats. In acute treatment studies in normal volunteers subjects received 9 tablets of the finished product Jarsin 300 and placebo in the pilot study (unblinded) and in the main study (a double blind, balanced order, cross-over design). Results in normal volunteer studies show that HP caused significant increases of salivary cortisol and plasma growth hormone (GH) whereas it decreased plasma prolactin versus placebo. Plasma hormone levels were associated with a rise in plasma hyperforin but not with hypericin, however no significant correlation was found. In the animal studies, acute treatment with LI 160, hyperforin and hypericin all caused significant increases in plasma corticosterone. This was associated with significant increases in brain cortical tissue 5-HT content. The corticosterone responses were attenuated by the 5-HT2 receptor antagonist, ketanserin but not by the 5-HT1A antagonist, WAY-100635. This suggests that the corticosterone responses may be mediated via a 5-HT2 mechanism of action. When sub-chronic and acute treatment using two different doses of LI 160 were compared, plasma corticosterone level were significantly decreased. Thus suggesting a down-regulation or desensitisation of post-synaptic 5-HT2 receptors. Plasma prolactin was significantly reduced by acute treatment with LI 160 and hyperforin treatment but not by hypericin. This was associated with a concomitant rise in brain cortical tissue DA. Both LI 160 and hyperforin treatments decreased the plasma prolactin responses to the DA antagonist, haloperidol, suggesting that this may be associated with a DA-mediated mechanisn of action. When acute and sub-chronic treatments were compared, plasma prolactin responses were increased in the sub-chronically treated animals. The studies when taken together suggest that the LI 160 extract may effect plasma hormonal changes via both 5-HT and DA-mediated mechanisms but do not involve noradrenaline (NA). The data also suggests that hyperforin may be more important than hypericin for effecting these changes following acute treatment. Further studies investigating both acute and sub-chronic effects of these compounds are necessary.

-----------------------------------


J Psychopharmacol 2000;14(4):360-3 Related Articles, Links


Acute effects of LI 160 (extract of Hypericum perforatum, St John's wort) and two of its constituents on neuroendocrine responses in the rat.

Franklin M, Chi JD, Mannel M, Cowen PJ.

University Department of Psychiatry, Warneford Hospital, Oxford, UK. michael.franklin@psych.ox.ac.uk

Extracts of Hypericum perforatum (St John's wort), such as LI 160, which are effective antidepressants have several active constituents. Their mode of action in depression, however, is unclear. In the present investigation, we assessed the effect of equivalent doses of LI 160 and two of its components, hypericin and hyperforin on serotonin (5-HT) and dopamine (DA)-mediated neuroendocrine responses in the rat. LI 160, hypericin and hyperforin significantly and equivalently increased plasma corticosterone. This effect was blocked by ketanserin but not WAY-100635, suggesting mediation via 5-HT2 receptors. LI 160 also lowered plasma prolactin and prevented the increase in plasma prolactin following haloperidol administration. Hyperforin had a similar but somewhat less pronounced effect. We conclude that LI 160, hypericin and hyperforin all increase 5-HT-mediated corticosterone release while LI 160 enhances DA-mediated inhibition of prolactin release. Hyperforin may contribute to the facilitatory effect of LI 160 on DA function, but hypericin does not.

---------------------------------


Biol Psychiatry 1999 Aug 15;46(4):581-4 Related Articles, Links


Neuroendocrine evidence for dopaminergic actions of hypericum extract (LI 160) in healthy volunteers.

Franklin M, Chi J, McGavin C, Hockney R, Reed A, Campling G, Whale RW, Cowen PJ.

University Department of Psychiatry, Warneford Hospital, Oxford, UK.

BACKGROUND: We studied the effect of a single dose of a formulation of a methanolic extract of Hypericum perforatum (HP), also known as St. John's wort, on plasma concentrations of growth hormone (GH), prolactin (PRL), and cortisol (CORT) in 12 healthy male volunteers. METHODS: Subjects received 9 tablets of the finished product Jarsin 300 and placebo in a double-blind, balanced-order, cross-over design. RESULTS: Following HP relative to placebo, there was a significant increase in plasma GH and a significant decrease in plasma PRL. Plasma CORT levels were unchanged. CONCLUSIONS: Taken together with data from animal experimental studies, the findings suggest that this dose of HP may increase some aspects

 

[Drveejay11]

LOL (Hhajdo---good for convo anyway..... ):

Part II:
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.

 

[hhajdo]

Yes, as it was written in the T-mag article, PRL increase is caused by estrogen so using aromatase inhibitors / antiestrogens will take care of it - check the studies in my previous post.
I don't think that using bromo with it is a good idea since it can negatively effect HPTA recovery.

I agree that low PRL may increase your sex drive, I've posted this study in your thread on Elite:


Int J Impot Res 2002 Apr;14(2):133-5 Related Articles, Links


Absence of orgasm-induced prolactin secretion in a healthy multi-orgasmic male subject.

Haake P, Exton MS, Haverkamp J, Kramer M, Leygraf N, Hartmann U, Schedlowski M, Krueger TH.

Department of Medical Psychology, University Clinic of Essen, Germany.

In several studies we have recently demonstrated that orgasm induces prolactin secretion in healthy males and females. This suggests that prolactin may form a feedback regulator of the refractory period following orgasm. To examine this position we investigated the prolactin response of a healthy multi-orgasmic male subject. Blood was drawn continuously during masturbation-induced orgasm. The prolactin response of the case-subject was compared with that of nine healthy adult men with a normal refractory period. The case-subject showed no prolactin response to three orgasms. Data from this multi-orgasmic subject support the hypothesized role of plasma prolactin in contributing to sexual-satiation mechanisms


Neurosci Biobehav Rev 2002 Jan;26(1):31-44 Related Articles, Links


Orgasm-induced prolactin secretion: feedback control of sexual drive?

Kruger TH, Haake P, Hartmann U, Schedlowski M, Exton MS.

Department of Medical Psychology, University of Essen, 45122 Essen, Germany.

Recent studies from our laboratory have investigated the hormonal response to various forms of sexual stimulation, including film, masturbation, and coitus in both men and women. This series of studies clearly demonstrated that plasma prolactin (PRL) concentrations are substantially increased for over 1h following orgasm (masturbation and coitus conditions) in both men and women, but unchanged following sexual arousal without orgasm. Here we discuss evidence suggesting that the PRL response to orgasm may play an important role in the control of acute sexual arousal following orgasm. Supporting this position, chronic elevations of PRL (hyperprolactinemia) produce pronounced reductions in animal sexual activity, and significant reduction of libido and gonadal function in both men and women. These data suggest that PRL may represent a peripheral regulatory factor for reproductive function, and/or a feedback mechanism that signals CNS centres controlling sexual arousal and behaviour. Thus, we propose a theoretical model of the role of PRL as a neuroendocrine reproductive reflex.

 

[Drveejay11]

I AM POSTING THIS PURELY FOR THE FUN OF SEEING HHAJDO GO CRAZY!

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. hoyang@ucla.edu

(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
levels?

There is only ONE mechanism:

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

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.....

I.E. YOU BEGIN TO LACTATE!!!!!

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

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. Winstrol (winny) would be the only help I would see with A-drol. That is one crazy substance.

 

[hhajdo]

LOL

 

[Drveejay11]

LOL......

 

[StoneColdNTO]

LOL......

Can you please explain your post in laymens terms, 500 words or less, would be nice !!