The PERFECT STEROID is:
- Highly ANDROGENIC
- Highly ANABOLIC
- Does not convert to Estrogen
- Does not convert to DHT
- Has no Progestational component
- Increases Mood
- Increases libido
- LIGHT on the HPTA
ENTER THE ANABOLIC REVOLUTION:
*HALOBOLAN*
Combining the PERFECT ANDROGENIC qualities of HALOTESTIN with the PERFECT ANABOLIC properties of PRIMOBOLAN, results is a SYNERGISTIC SMASH of muscle and strength EXPLOSION!
Halotestin is the single best STRENGTH-inducing compound on a mg for mg basis. DESPITE BEING SO ANDROGENIC, it has virtually NO effect on the HPTA!* It does not convert to Estrogen or progesterone, and in fact, is actually ANTI-estrogenic. To top things off, Halotestin will make you feel like a SUPERMAN that hasn't been laid in YEARS! Great for Libido and mood! BUT, lacking the A-R binding affininty that PRIMO has, used on it's own, it is not very effective for optimal mass-gain.
PRIMOBOLAN needs no introduction at all. Primobolan binds to the Androgen-receptor even BETTER THAN TESTOSTERONE. Primobolan is HIGHLY ANABOLIC, though, lacking a STRONG ANDROGENIC component. Ergo, used by itself, it is not very effective for building TONS of muscle. Like HALO however, it is not very supressive of endogenous testosterone production(used in NORMAL dosages; 300-400mgs), and it does not undergo conversion to either estrogen or DHT.
Combining Halotestin in Primobolan gives you the BEST OF BOTH WORLDS. Since there is thusfar NO steroid containing such a ratio WITHOUT also being estrogenic or progestational, we must MAKE ONE.
For those seeking TIME OFF of HEAVY COMPOUNDS that supress the HPTA, HALOBOLAN will serve as a great alternative, allowing still for GREAT STRENGTH AND MUSCLE-MASS GAINS!
Weeks 1-6: Halotestin, 20mgs
Weeks 1-6: Oral Primobolan, 100mgs ED
Halobolan is a 6 week cycle, as Halotestin is particulalry hard on the liver. I also kept the dosage to the minimum. Primobolan is NOT liver toxic but has a poor bioavailability rate, so the 100mg's ED is justified.
Expect INSANE STRENGTH, INCREDIBLE MUSCLE HARDNESS, and TONS OF LEAN-TISSUE!
Since anabolic steroids first made their GRAND appearance in the ealry 1900's, they have been rapidly evolving since.
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NOT ALL ANDROGENS CAUSE SHUTDOWN*
"Shutdown", is defined by a COMPLETE inhibition of the Pituitary/Testes, resulting in a TOTAL cessation of endogenous androgen production.
SOME androgens will only SUPPRESS endogenous androgen production, resulting in a DECREASED testosterone level, but not a complete shutdown. (Tbol, Var, Wistrol, EQ, Dianabol, masteron, proviron, halo, primo)
Very Androgenic/Progestenic/Estrogenic steroids(Tren, Deca, Drol, Test) cause a COMPLETE shutdown of endogenous hormone production.
The distinction between SUPRESSION and SHUTDOWN is utterly important, as steroids that cause LESS supression of endogenous hormones will allow for greater retention of gains upon ending the cycle, and a quicker, easier PCT.
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Horm Metab Res. 1984 Sep;16(9):492-7.Related Articles, Links
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.
Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.
We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased. Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL. There was, however, a reduction in the integrated and incremental TSH secretion after TRH. Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged. In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH. Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.(ABSTRACT TRUNCATED AT 250 WORDS
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