Bromocriptine vs. FinaDick

  1. Bromocriptine vs. FinaDick

    From Terminator76

    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.

    got more info regarding prolactin. This one I got from

    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.

    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

  2. Very good post YJ.. I swear you must be reading my mind.. everytime I am about to ask a question you post the answer before I get to write the question

    Has anyone used bromo with tren on cycle? I would like to here about your experiences if you have.. both positive and negative.

  3. Hey YJ i have been thinking on this shut down process, could it be that some guys are over doing dosages? if there whole system is getting that far out of whack to the point of prolacting and gyno is this just a bit to much or is this where we want to be for Maximum growth potential?

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