Please Scroll Down to See Forums Below prolactin is used in both male and females to promote the body to produce testosterone only, it doesnt aid in neorotransmittance or blocking, progesterone is an estrogen blocker and it reduces the the onset and effects as well as the production of estro. prolactin is a better choice when dealing with first timers, its easier to jump start their system. For experienced and perennial users one should consider a both. hope this helps.
You also need to consider that back in the day the Internet was not around. Tren is easily obtained and allot of people are trying it. Just look at the shear volume of post on this board alone.
Coincidentally my case of Gyno occurred of 75 mg EOD around week five. This is my second case the first was from puberty and was exacerbated by a deca, winny, test cycle. Had it removed and it looked great. Now I' having Gyno surgery # 2 this year. I think it is wise to make the assumption that if you have ever had real gyno removed or still have, then Tren is not a wise choice given that it effects the endocrine system on multiple levels. For those who do not have a problem it is a great drug. For those who do, you are playing with fire and your libel to get burnt. I did.. But then again I did not know any better even with my extensive medical education. Now I know but what an expensive lesson to learn.
Coincidentally my case of Gyno occurred of 75 mg EOD around week five. This is my second case the first was from puberty and was exacerbated by a deca, winny, test cycle. Had it removed and it looked great. Now I' having Gyno surgery # 2 this year. I think it is wise to make the assumption that if you have ever had real gyno removed or still have, then Tren is not a wise choice given that it effects the endocrine system on multiple levels. For those who do not have a problem it is a great drug. For those who do, you are playing with fire and your libel to get burnt. I did.. But then again I did not know any better even with my extensive medical education. Now I know but what an expensive lesson to learn.
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.
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.
Unfortunately, the authors of the paper described below do not state which anabolic steroids were used, but did note a significant drop in serum thyroid hormone levels.
Am J Sports Med 1987 Jul-Aug;15(4):357-61
Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.
Alen M, Rahkila P, Reinila M, Vihko R.
Department of Health Sciences, University of Jyvaskyla, Finland.
Endocrine responses in seven power athletes were investigated during a 12 week strength training period, when the athletes were taking high doses of androgenic-anabolic steroids, and during the 13 weeks following drug withdrawal. During the use of steroids significant decreases (P less than 0.05 to 0.001) in the serum concentrations of thyroid stimulating hormone, thyroxine, triidothyronine, free thyroxine, and thyroid hormone-binding globulin (TBG) were found, whereas the value of triidothyronine uptake increased (P less than 0.001). In relation to the changes in the thyroid function parameters measured, we suggest that the primary target of androgen action was TBG biosynthesis. In five of the seven subjects, serum concentrations of growth hormone increased at some point of the study 5 to 60-fold. Because of the use of exogenous testosterone, serum testosterone concentration tended to increase. This increase was associated with a corresponding increase (P less than 0.001) in serum estradiol. Furthermore, there were major decreases in
serum LH (P less than 0.01) and FSH (P less than 0.01) concentrations, and testicular testosterone production was therefore decreased. This was characterized by a very low serum testosterone concentration (5.1 +/- 1.8 nmol/l) 4 weeks following drug withdrawal. Cessation of drug use resulted in return of all the variables measured to the initial values, except for serum testosterone, which was at a low level (14.6 +/- 8.8 nmol/l) 9 weeks after drug withdrawal, indicating prolonged impairment of function. No consistent changes were found in the eight control athletes.
Am J Sports Med 1987 Jul-Aug;15(4):357-61
Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes.
Alen M, Rahkila P, Reinila M, Vihko R.
Department of Health Sciences, University of Jyvaskyla, Finland.
Endocrine responses in seven power athletes were investigated during a 12 week strength training period, when the athletes were taking high doses of androgenic-anabolic steroids, and during the 13 weeks following drug withdrawal. During the use of steroids significant decreases (P less than 0.05 to 0.001) in the serum concentrations of thyroid stimulating hormone, thyroxine, triidothyronine, free thyroxine, and thyroid hormone-binding globulin (TBG) were found, whereas the value of triidothyronine uptake increased (P less than 0.001). In relation to the changes in the thyroid function parameters measured, we suggest that the primary target of androgen action was TBG biosynthesis. In five of the seven subjects, serum concentrations of growth hormone increased at some point of the study 5 to 60-fold. Because of the use of exogenous testosterone, serum testosterone concentration tended to increase. This increase was associated with a corresponding increase (P less than 0.001) in serum estradiol. Furthermore, there were major decreases in
serum LH (P less than 0.01) and FSH (P less than 0.01) concentrations, and testicular testosterone production was therefore decreased. This was characterized by a very low serum testosterone concentration (5.1 +/- 1.8 nmol/l) 4 weeks following drug withdrawal. Cessation of drug use resulted in return of all the variables measured to the initial values, except for serum testosterone, which was at a low level (14.6 +/- 8.8 nmol/l) 9 weeks after drug withdrawal, indicating prolonged impairment of function. No consistent changes were found in the eight control athletes.
Swoleyoley
New member
no one has said anything that is a fact
perfectspecimen
New member
we are getting a lot of conficts here.
1. will taking arimidex and vitex prevent gyno
2. or will taking arimidex and bromo work
3. arimidex and nolvadex
4. arimidex and deprenyl
5. arimidex vitex nolvadex and bromo
which one would be the best choice and still not hinder gains too much?
so do people get gyno from vitex or ru-486?
will ru-486 prevent fina gyno?
1. will taking arimidex and vitex prevent gyno
2. or will taking arimidex and bromo work
3. arimidex and nolvadex
4. arimidex and deprenyl
5. arimidex vitex nolvadex and bromo
which one would be the best choice and still not hinder gains too much?
so do people get gyno from vitex or ru-486?
will ru-486 prevent fina gyno?
perfectspecimen
New member
how about taking
arimidex 1mg/ed
vitex 1.5g/ed
ru-486 20mg/eod
deprenyl 10mg/ed
will that take care of the gyno from fina?
arimidex 1mg/ed
vitex 1.5g/ed
ru-486 20mg/eod
deprenyl 10mg/ed
will that take care of the gyno from fina?
blaster220
New member
Been 5 days... where's Fonz 
Looking forward to reading up!
Looking forward to reading up!Similar threads
