Masteron / Drostanolone Propionate Effective Dosages Profile. 100mg/ml

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[h=1]Masteron[/h]Pro Anabolic Steroid Masteron
MA-01-Maxpro-Mastern-100-100mg-per-ml-10ml-vial-148x148.jpg

Product Name: Masteron 100
Substance: Drostanolone Propionate
Manufacturer: Maxpro
Content: 100mg per ml - 10ml vial
Effective Dose: 100mg every other day

Masteron / Drostanolone Propionate had formerly been a rare drug in the United States and was enjoyed principally by our European friends. This was due to never been produced in great quantity by Syntex and never being marketed in the United States. It presently is available from various non-pharmaceutical suppliers. Many also make home-prepared injectables from powder provided by various sources.
Masteron is unaffected by the aromatase and 5alpha-reductase enzymes and therefore there are no issues with estrogen or with potentiation (increase of effect) in tissues such as the skin and prostate. In fact, Masteron is somewhat anti-estrogenic due to competing with estradiol at the estrogen receptor, while not itself activating the receptor, and perhaps by likewise competing with testosterone for the binding site of the aromatase enzyme, thus reducing conversion.
This is a benefit when only a moderate amount of aromatizing steroids are used and no other anti-estrogen is used. It is not, however, sufficient to fully deal with high doses of aromatizing steroids, or at least not with typical doses of Masteron; and is unnecessary when more effective anti-estrogens are employed.
But estrogen control is not the main benefit of Masteron. It is an effective Class I anabolic that is low in adverse side effects. While it has wrongly been accused of being a weak anabolic, due to at least two factors involved which have confused the issue, it in fact has rather typical potency.
The first such factor is that a conclusion of weakness is usually made at low doses at which few anabolic steroids excel. The usually-provided concentrations tend to lead to usages of 350 mg/week or an even smaller amount. Anabolic steroids generally are not tremendously powerful at 350 mg/week, whether individually or even in combination, so it really is no testament against Masteron that it does not burn the house down at that dosage.
Use at 700 mg/week or a gram per week is entirely reasonable, and with a more substantial dosage such as this, Masteron performs quite satisfactorily.
In the event that a user does not wish to use quite this much due to expense or availability, it of course is possible – though contrary to the human tendency to favor round numbers -- to inject amounts such as 75 mg per day, or 150 mg every other day, which totals to 525 mg/week. This is not maximally effective, but provides a very worthwhile improvement compared to 350 mg/week.
A second reason for underestimation of the potency of Masteron is neglecting that no Class I steroid gives maximal results without a complementary Class II compound being used concurrently. This drug is no exception.
For higher dose use, if not otherwise using any other aromatizable steroid in combination, adding at least a small amount of testosterone to be sure of maintaining normal estrogen levels. Alternately, low-dose HCG use may be employed.
Masteron is a useful substitute for either trenbolone or Primobolan.
A property that Masteron shares with Primobolan, but which differs from trenbolone, is that it has relatively little tendency to suppress the HPTA when used at low doses. I have not yet established how high a dose may be used while maintaining only minimal inhibition of natural testosterone, but 100 mg/week is usable and very noticeably beneficial off-cycle. Recommend that it not be employed until natural testosterone production is fully restored, however.
Masteron has been favored for cutting, for which it is indeed useful, but not required as there are other anabolic steroids which are similarly effective for the purpose.
While ordinarily there is no particular point in using more than one Class I steroid in a stack, as none of them do a job at building muscle that the others do not, where one is concerned about side effects that are particular to another Class I steroid being used, it can make sense to use a more moderate dose of that steroid and to employ Masteron for the remainder of the desired Class I activity. In this case, as the other such compound will also be contributing substantially to providing this activity, a moderate Masteron dose such as 100 mg every other day can yield sufficient total such effect.
Or as it the case with almost all anabolic steroids, Masteron can be profitably added to testosterone, generally without adding noticeable side effects.
Drostanolone Propionate is the chemical name of active ingredient in Masteron. Masteron was a registered trademark of Sarva-Syntex in Belgium and/or other countries prior to cancellation.
 
I think the reason why Masteron is minimally inhibitory - is because it has direct aromatase inhibiting effects and directly opposes the estrogen receptor with a high affinity.
Based on my research, the only other way DHT inhibits the hypothalamus, besides through CROSS-ACTIVATION of estrogen-receptor BETA (and subsequent activation of GABA-A activity), is through beta-endorphin release - though DHT actually opposes other opioid receptors ----so you would only need a kappa opioid antagonist to minimize or eliminate the HPTA inhibition......so something like a GABA-A antagonist; but don't block GABA-B obviously, and then a kappa antagonist, something like amentoflavone would work.
7,8 Benzoflavone, or kudzu extract could block GABA-A pretty potently , but is not advised for those susceptible to anxiety ; especially social anxiety!

TAMOXIFEN, AS SEEN BELOW, PLUS 7,8 BENZOFLAVONE, AND THEN AMENTOFLAVONE WOULD ELIMINATE OR REDUCE THE HPTA INHIBITION BY DHT COMPOUNDS.

The Androgen 5α-Dihydrotestosterone and Its Metabolite 5α-Androstan-3β, 17β-Diol Inhibit the Hypothalamo–Pituitary–Adrenal Response to Stress by Acting through Estrogen Receptor β-Expressing Neurons in the Hypothalamus



  • [*=left]Trent D. Lund,
    [*=left]Laura R. Hinds, and
    [*=left]Robert J. Handa
+Show Affiliations



  1. [*=left]<cite style="margin: 0px; padding: 0px; border: 0px; outline-style: none; font-style: normal; font-size: 11px; font-family: inherit; line-height: inherit; text-align: inherit; vertical-align: baseline; display: block;">26(5): 1448-1456; doi: 10.1523/JNEUROSCI.3777-05.2006</cite>





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Abstract


Estrogen receptor β (ERβ) and androgen receptor (AR) are found in high levels within populations of neurons in the hypothalamus. To determine whether AR or ERβ plays a role in regulating hypothalamo–pituitary–adrenal (HPA) axis function by direct action on these neurons, we examined the effects of central implants of 17β-estradiol (E2), 5α-dihydrotestosterone (DHT), the DHT metabolite 5α-androstan-3β, 17β-diol (3β-diol), and several ER subtype-selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization stress. In addition, activation of neurons in the paraventricular nucleus (PVN) was monitored by examining c-fos mRNA expression. Pellets containing these compounds were stereotaxically implanted near the PVN of gonadectomized male rats. Seven days later, animals were killed directly from their home cage (nonstressed) or were restrained for 30 min (stressed) before they were killed. Compared with controls, E2 and the ERα-selective agonists moxestrol and propyl-pyrazole-triol significantly increased the stress induced release of corticosterone and ACTH. In contrast, central administration of DHT, 3β-diol, and the ERβ-selective compound diarylpropionitrile significantly decreased the corticosterone and ACTH response to immobilization. Cotreatment with the ER antagonist tamoxifen completely blocked the effects of 3β-diol and partially blocked the effect of DHT, whereas the AR antagonist flutamide had no effect. Moreover, DHT, 3β-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN. Together, these studies indicate that the inhibitory effects of DHT on HPA axis activity may be in part mediated via its conversion to 3β-diol and subsequent binding to ERβ.
 
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