Bromocriptine vs. FinaDick
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.
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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. Winny would be the only help I would see with A-drol. That is one crazy substance.
Peace
Posted by Trenimator76 on 01-22-2003 04:13 PM:
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.
__________________
I do not use any illegal substances or promote the use of anabolic steroids without a doctor's prescription. The information I share is for entertainment purposes only.
Posted by Trenimator76 on 01-23-2003 08:43 AM:
Crazy for Bromocriptine, or just Crazy?
Bromocriptine is sold within the United States by Novartis under the tradename, Parlodel®. Bromocriptine is a long acting dopamine (D2) receptor agonist, primarily used to treat Parkinson’s disease.
In animals, bromocriptine has been found to lower blood sugar levels, reduce circulating free fatty acids, and to reduce food intake by 55%. In humans, similar effects have been found, with the major side effect being blinding headaches.
In a two-year human study, bromocriptine caused a weight loss of ~13 kilograms (which was more than 10% of subjects' body weight). As stated earlier, bromocriptine affects the D2 receptor and this receptor has been associated with the "reward deficiency syndrome," namely because people with certain addictions have defective D2 receptors.
It appears that compulsive eating may fit into this dopaminergic syndrome and that bromocriptine at the right dose may be just what the doctor ordered. However, keep in mind that bromocriptine doesn't just work by curbing the appetite, but by lowering the aformentioned free fatty acids and lowering blood sugar, too.
Besides bromocriptine, a similar acting drug known as cabergoline (made by Pharmacia) is being investigated as a weight loss treatment
__________________
I do not use any illegal substances or promote the use of anabolic steroids without a doctor's prescription. The information I share is for entertainment purposes only.
Posted by hhajdo on 02-18-2003 06:28 PM:
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.
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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
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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.
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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.
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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.
[email protected]
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.
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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
Posted by Huge285 on 01-31-2004 08:52 AM:
I find all this research data and the inferences made from the studies to be very interesting.........it really made me think. In summary, this is what i concluded,
(1)Increased DOPAMINE--->Decreased Prolactin--->Decreased TEST
(2)Increased ESTROGEN--->Increased Prolactin
(3)TRH--->Increased Prolactin--->Galactorrhea (gyno)
(4)Bromocriptine (synthetic Dopamine)--->Decreased Prolactin (cures the Prolactin-induced gynecomastia)
............HOWEVER, when Trenimator76 concluded that TRENBOLONE might exert its Anti-glucocorticoid effects by reducing the amount of TSH (and thus T3 and T4).......i have to disagree. The term anti-glucocorticoid refers to a reduction in serum cortisol levels (not a reduction in THYROID HORMONE (T4 and T3). Reducing THYROID hormone might actually slow down protein synthesis (not many people lose muscle because their body is producing too much THyroid-- maybe if they produced too much cortisol))
Extrapolating from the ST JOHNS WORT study, Perhaps TRENBOLONE Decreases brain 5-HTP (SEROTONIN) which in turn DECREASES Serum CORTISOL. If TREN can reduce brain 5-HTP levels, PERHAPS it also reduces brain DOPAMINE levels which in turn increase PROLACTIN levels (thus causing your prolactin-induced gynecomastia)?
