Tren: finasteride and an anti-prolactin on cycle
- 12-27-2005, 09:20 PM
Tren: finasteride and an anti-prolactin on cycle
Alright guys, been browsing over this topic for the last hour or so, and felt the need to start a new thread (I know yall just love me for it too )
Anyway, my next cycle will incorporate test pretty much throughout (prop or enanthate) with tren up front, EQ starting a couple weeks in and masteron after tren ace. I will also be using M4OHN to back load with the masteron. I was planning on running some saw palmetto and low dose finasteride (.5 mg/day) to prevent hair loss and prostate issues, especially from the tren and masteron. I will also be running low dose arimidex as needed. Now I have read some concerns with taking fina with deca, though some say it is a myth.
My other question is what people recommend for possible prolactin issues, bromo or dostinex.
Any advice is appreciated guys...
- 12-28-2005, 12:10 AM
Dostinex is a better choice while on cycle. Off cycle however, bromo is a better choice.
I would seriously recommend not touching finasteride with a 40 foot pole. It is now known to cause permanent libido loss in many people. It's just not worth the risk.
Also, finasteride will not help with the sides from tren. It will only help with the test, and I suspect the help it provides is moderate at best.
And that sounds like a big heap of drugs. Why not use test + tren and call it a day?
12-28-2005, 12:45 AM
starting with test and tren and ending with mast and test. The EQ adds a nice anabolic kick to this cycle, and at its price, you really cannot go wrong with EQOriginally Posted by rhinochaser48
After smelling some of the topical hair loss prods, I will NOT go towards them with a 10 ft pole. I have heard that low dose proscar (.5 mg) is low in terms of sides. What other options does one have for hair loss. I love my hair damnit, lol.
Lastly, any recs on dostinex dosages.
12-28-2005, 01:23 AM
Originally Posted by Max32
Sorry, it's been awhile since I reviewed the info on dostinex.
I tried some topical spironlactone a couple of years ago and it didn't smell bad. I got it from www.wholesalehairproducts.com.
I don't blame you for trying to keep your hair though.
I gave up trying to keep mine. I started losing it before my first cycle at age 21. My mother's brother was the same. He had a crown bald spot at 21 also. Now I just shave it all since fighting this portion of my genetics is lost cause.
12-28-2005, 02:47 AM
@ max 32 nice cycle you got there... I've been researching on dostinex and prolactin issues while being on deca or tren as well, but I'm speculating on the fact that dostinex blocks ENDOGENOUS prolactin secretion, and I don't know if progestins AAS will raise pituitary prolactin output (by binding to PRL receptors I assume).If it's the case, then a drug like dostinex will do the trick as it will lowers prolactin efficiently, but if it doesn't raise endo prolactin levels, then a progesterone blocker would be better in theory, but it's expensive.Also I think you know that Dostinex is supposed to give you a crazy libido and that's always good.
0.5mg twice weeklyLastly, any recs on dostinex dosages.
and here's what you need to know about dostinex ...
Pharmaceutical name : Cabergoline
Chemical formula : 1-[(6-allylergolin-8(beta)-yl)-carbonyl]-1-[3-(dimethylamino)propyl]-3-ethylurea
Drug Class: dopamine receptor (D2) agonist / anti prolactin
CLINICAL PHARMACOLOGY :
• Mechanism of Action:
The secretion of prolactin by the anterior pituitary is mainly under hypothalamic inhibitory control, likely exerted through release of dopamine by tuberoinfundibular neurons. Cabergoline is a long-acting dopamine receptor agonist with a high affinity for D 2 receptors. Results of in vitro studies demonstrate that cabergoline exerts a direct inhibitory effect on the secretion of prolactin by rat pituitary lactotrophs. Cabergoline decreased serum prolactin levels in reserpinized rats. Receptor-binding studies indicate that cabergoline has low affinity for dopamine D 1 , (alpha) 1 - and (alpha) 2 -adrenergic, and 5-HT 1 - and 5-HT 2 -serotonin receptors.
• Clinical Studies:
The prolactin-lowering efficacy of DOSTINEX was demonstrated in hyperprolactinemic women in two randomized, double-blind, comparative studies, one with placebo and the other with bromocriptine. In the placebo-controlled study (placebo n=20; cabergoline n=168), DOSTINEX produced a dose-related decrease in serum prolactin levels with prolactin normalized after 4 weeks of treatment in 29%, 76%, 74% and 95% of the patients receiving 0.125, 0.5, 0.75, and 1.0 mg twice weekly respectively.
In the 8-week, double-blind period of the comparative trial with bromocriptine (cabergoline n=223; bromocriptine n=236 in the intent-to-treat analysis), prolactin was normalized in 77% of the patients treated with DOSTINEX at 0.5 mg twice weekly compared with 59% of those treated with bromocriptine at 2.5 mg twice daily. Restoration of menses occurred in 77% of the women treated with DOSTINEX, compared with 70% of those treated with bromocriptine. Among patients with galactorrhea, this symptom disappeared in 73% of those treated with DOSTINEX compared with 56% of those treated with bromocriptine.
Following single oral doses of 0.5 mg to 1.5 mg given to 12 healthy adult volunteers, mean peak plasma levels of 30 to 70 picograms (pg)/mL of cabergoline were observed within 2 to 3 hours. Over the 0.5-to-7 mg dose range, cabergoline plasma levels appeared to be dose-proportional in 12 healthy adult volunteers and nine adult parkinsonian patients. A repeat-dose study in 12 healthy volunteers suggests that steady-state levels following a once-weekly dosing schedule are expected to be twofold to threefold higher than after a single dose. The absolute bioavailability of cabergoline is unknown. A significant fraction of the administered dose undergoes a first-pass effect. The elimination half-life of cabergoline estimated from urinary data of 12 healthy subjects ranged between 63 to 69 hours. The prolonged prolactin-lowering effect of cabergoline may be related to its slow elimination and long half-life.
In animals, based on total radioactivity, cabergoline (and/or its metabolites) has shown extensive tissue distribution. Radioactivity in the pituitary exceeded that in plasma by >100-fold and was eliminated with a half-life of approximately 60 hours. This finding is consistent with the long-lasting prolactin-lowering effect of the drug. Whole body autoradiography studies in pregnant rats showed no fetal uptake but high levels in the uterine wall. Significant radioactivity (parent plus metabolites) detected in the milk of lactating rats suggests a potential for exposure to nursing infants. The drug is extensively distributed throughout the body. Cabergoline is moderately bound (40% to 42%) to human plasma proteins in a concentration-independent manner. Concomitant dosing of highly protein-bound drugs is unlikely to affect its disposition.
In both animals and humans, cabergoline is extensively metabolized, predominately via hydrolysis of the acylurea bond or the urea moiety. Cytochrome P-450 mediated metabolism appears to be minimal. Cabergoline does not cause enzyme induction and/or inhibition in the rat. Hydrolysis of the acylurea or urea moiety abolishes the prolactin-lowering effect of cabergoline, and major metabolites identified thus far do not contribute to the therapeutic effect.
After oral dosing of radioactive cabergoline to five healthy volunteers, approximately 22% and 60% of the dose was excreted within 20 days in the urine and feces, respectively. Less than 4% of the dose was excreted unchanged in the urine. Nonrenal and renal clearances for cabergoline are about 3.2 L/min and 0.08 L/min, respectively. Urinary excretion in hyperprolactinemic patients was similar.
Dose response with inhibition of plasma prolactin, onset of maximal effect, and duration of effect has been documented following single cabergoline doses to healthy volunteers (0.05 to 1.5 mg) and hyperprolactinemic patients (0.3 to 1 mg). In volunteers, prolactin inhibition was evident at doses >0.2 mg, while doses >/=0.5 mg caused maximal suppression in most subjects. Higher doses produce prolactin suppression in a greater proportion of subjects and with an earlier onset and longer duration of action. In 12 healthy volunteers, 0.5, 1, and 1.5 mg doses resulted in complete prolactin inhibition, with a maximum effect within 3 hours in 92% to 100% of subjects after the 1 and 1.5 mg doses compared with 50% of subjects after the 0.5 mg dose.
In hyperprolactinemic patients (N=51), the maximal prolactin decrease after a 0.6 mg single dose of cabergoline was comparable to 2.5 mg bromocriptine; however, the duration of effect was markedly longer (14 days vs 24 hours). The time to maximal effect was shorter for bromocriptine than cabergoline (6 hours vs 48 hours).
In 72 healthy volunteers, single or multiple doses (up to 2 mg) of cabergoline resulted in selective inhibition of prolactin with no apparent effect on other anterior pituitary hormones (GH, FSH, LH, ACTH, and TSH) or cortisol.
Initial doses higher than 1.0 mg may produce orthostatic hypotension. Care should be exercised when administering DOSTINEX with other medications known to lower blood pressure.
• Postpartum Lactation Inhibition or Suppression:
DOSTINEX is not indicated for the inhibition or suppression of physiologic lactation. Use of bromocriptine, another dopamine agonist for this purpose, has been associated with cases of hypertension, stroke, and seizures.
• Hepatic Impairment:
Since cabergoline is extensively metabolized by the liver, caution should be used, and careful monitoring exercised, when administering DOSTINEX to patients with hepatic impairment.
• Drug Interactions:
DOSTINEX should not be administered concurrently with D 2 -antagonists, such as phenothiazines, butyrophenones, thioxanthenes, or metoclopramide.
12-28-2005, 04:01 PM
03-02-2006, 11:23 AM
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