What do you guys think about the new prohormone by syntrax “pentabol Extreme.” Its different from the old one, they have added an ether to it making it more accesible for the body to use taken orally. Let me know what you guys think about it.
I think that’s the one Brock talked about in his last column. Here it is:
Q: I was wondering what your opinion was regarding the new
17-b ether prohormones that were launched within the last
week or so? The logic behind them seems pretty solid and I
was wondering how they would stack up against the new
Biotest 4-AD-EC?
A: Hormones with an ether group in the 17-b position are not new (even if They are not popular anywhere outside of Japan). The steroid "quinbolone" comes to my mind when I think of a legit anabolic steroid that has an ether group at on the 17-b. Quinbolone was sold under the brand name "Anabolicum Vister" in the 1970's.
It was never a popular steroid because despite this "miracle
breakthrough," of adding an an ether group to position 17-b
to increase oral bioavailability, it still took a lot of quinbolone
to see even a mild anabolic effect.
Currently, the only company making a 17-b steroidal ether is
Shionogi of Japan who make a drug called mepitiostane. The
3 or 4 people over the last decade or so whom I have spoken
to who have used this drug have all said it was a waste of
time. Bill Roberts and myself actively explored making 17-b
prohormone ethers but we abandoned the idea because they
don't really work any better than plain old prohormones do
and they cost a lot more. After we abandoned this idea, the
company currently marketing a 17-b prohormone ether
managed to find out about the technology from an overseas
vendor of ours who probably should have kept his mouth shut
but didn't. In any event, they decided to run with our
leftovers.
17-b ether technology works by causing the steroid/ether
compound to be picked up by the lymphatic system rather
than through the traditional route of absorption when you
take something orally. If this mechanism of action sounds
familair to you, it's because there is the non-17-b ether drug
called Andriol (testosterone undecanoate) which also works
this way — "work" being a highly subjective term because if
you ask most bodybuilders what they think of Andriol, a
universal "it sucks donkey balls" is what you'll hear as a reply.
To see any effects with Andriol, you'd need to take 8 of the
little brown gel caps (or 400mg) per day. I would not expect
that any 17-b ether prohormone would work anybetter than
Andriol does and in fact (as you will see), I think the current
product is utter crap. I think the 17-b ether prohormone is a
nice, shiny gimmick that really doesn't offer much over plain,
old prohormones. Still, you can't polish a turd.
The other issue is that the company making this 17-b ether
prohormone is making a 5-androstenediol and not a
4-androstenediol product. 5-androstenediol is all but useless
in building mass as less than 1% of it converts to
Testosterone and it deifinitely has some estrogenic side
effects that make it a poor choice for all men. I have no idea
why this company opted for a 5-androstenediol version when
they could have just as easily had a 4-androstenediol version
made. My opinion is that the R&D team at that company is a
bunch of no talent hacks who have stolen every single one
of their product ideas from a handful of other people at
competing companies over the last few years.
Comparing Biotest's 4-AD-EC to this crappy, 17-b ether 5-AD
would be a lot like picking on a mentally challenged kid — it's
not fair and it is not really all that fun. I would strongly
caution you to avoid this 17-b ether 5-AD product (if the
manufacturer makes a 4-AD version and you want to try it,
well heck, that's OK but I would avoid the current version like
the plague).
It is absolute crap!!! And it is estrogenic
as hell. 5-AD sucks. I have 4 references
that correlate high 5-AD levels to
pseudohermaphroditism in men. Plus, the
pentyl ether technology is a waste and just
a slick gimmick, Bill and I investigated this
over a year ago and we dropped it. This
guys stole the idea from us. Read these
studies and see how the maker of this
shit lies like a rug. 5-AD sucks. It is
marginally anabolic, hardly converts to
testosterone and is totally estrogenic.
See below:
Cancer Res 1982 Nov;42(11):4797-4800 Related Articles, Books,
Effects of aminoglutethimide on delta 5-androstenediol metabolism in postmenopausal women with breast cancer.
Bird CE, Masters V, Sterns EE, Clark AF.
delta-5-Androstene-3 beta, 17 beta-diol has potential estrogenic activity because it is known to bind to receptors and translocate to the nucleus of certain estrogen target tissues. We studied delta 5-androstene-3 beta, 17 beta-diol metabolism in postmenopausal women with breast cancer before and during aminoglutethimide-plus-hydrocortisone therapy, utilizing the constant infusion technique. The metabolic clearance rate for five subjects was 799 +/- 89 liters/24 hr (470 +/- 47 liters/24 hr/sq m) before and 751 +/- 93 liters/24 hr (444 +/- 57 liters/24 hr/sq m) during therapy. Plasma delta 5-androstene-3 beta, 17 beta-diol and delta 5-androstene-3 beta, 17 beta-diol free index decreased despite absence of change in the metabolic clearance rate. Increased dehydroepiandrosterone/delta 5-androstene-3 beta, 17 beta-diol conversion ratios in individual patients suggested an increase in 17 beta-hydroxysteroid dehydrogenase activity during therapy. There were no alterations in the formation of the estrogen precursors testosterone and delta 4-androstene-3,17-dione.
5-AD stimulates the growth of estrogen dependent breast cancers!!!
Ann Endocrinol (Paris) 1979;40(6):547-548 Related Articles, Books
[In vitro studies of testicular biosynthesis in 4 cases of male pseudohermaphrodism (MPH) due to testicular 17 ketoreductase defect (author’s transl)].
[Article in French]
de Peretti E, Cadillon E, Bertrand J.
In 3 cases of MPH due to 17-ketosteroid reductase defect, the pattern of testicular biosynthesis studied after incubating homogenates of testicular tissue with 14C-Progesterone and 3H-Pregnenolone was very similar. The most striking finding was the excessive production of delta 4-Androstenedione contrasting with the small amount of testosterone formed. Conversion of DHA to delta 5-Androstenediol was also limited. In addition, 3 pairs of substrates, namely 14C-testosterone and 3H-delta 4-androstenedione; 14C-estradiol and 3H-estrone; 14C-delta 5-androstenediol and 3H-DHA, were incubated for various length of time. Homogenates of testicular tissue from 2 cases presenting with the biosynthetic defect were studied as to compare to testicular tissues from 2 subjects with normal testicular biosynthesis. Different degrees in the impairment of the reduction or the oxydation were observed for the different pairs of substrates in pathological as well as in normal tissues. This suggests that the extent of the enzyme defect would differ for the 3 pairs of substrates.
J Clin Endocrinol Metab 1992 Sep;75(3):773-778 Related Articles, Books, LinkOut
Mechanisms of androgen production in male pseudohermaphroditism due to 17 beta-hydroxysteroid dehydrogenase deficiency.
Rosler A, Belanger A, Labrie F.
Department of Endocrinology and Metabolism, Hebrew University-Hadassah Medical Center, Jerusalem, Israel.
17 beta-Hydroxysteroid dehydrogenase (17 beta HSD) deficiency is a rare cause of male pseudohermaphroditism, but is a frequent disorder among a highly inbred Arab population in the Gaza strip. Affected individuals are born and reared as females until puberty, when marked virilization occurs, leading in many cases to the spontaneous adoption of a male gender role. To investigate the mechanisms and site(s) of androgen production, we determined the gonadal and extragonadal steroid patterns in two postpubertal male pseudohermaphroditism patients, who were castrated and reared as females. Before castration, both patients had very high plasma levels of androstenedione (delta 4-A), normal or moderately low levels of testosterone (T), and significantly elevated delta 4-A/T ratios (P less than 0.01). Dihydrotestosterone (DHT) levels were normal or high, while the DHT/T ratios were lower than normal (P less than 0.01), suggesting enhanced 5 alpha-reductase activity. These abnormalities were much more severe in spermatic venous blood. 17 beta HSD deficiency was also found in the delta 5-pathway, by high dehydroepiandrosterone (DHEA) levels and very high dehydroxyepiandrosterone/delta 5-androstenediol (DHEA/delta 5-diol) ratios, and in peripheral tissue metabolites, by very high androsterone glucuronide/3 alpha-androstanediol glucuronide ratios (P less than 0.01). The estrogen pathway was also impaired (P less than 0.01), even though both estrone and estradiol levels were elevated. Gonadectomy significantly reduced all androgens and estrogens (P less than 0.01), but when compared to 42 castrated controls, both patients had lower delta 4-A and higher T levels. The delta 4-A/T ratio was lower than that in controls, indicating normal to enhanced extragonadal 17 beta HSD activity. A similar pattern was observed in the delta 5- and estrogen pathways. DHT levels were within normal limits, and 3 alpha-diol was moderately decreased. These data suggest that testicular 17 beta HSD activity is under a different genetic control from that in extragonadal tissues. Affected males lack the testicular enzyme, but their extragonadal 17 beta HSD activity is normal or enhanced. Together with enhanced 5 alpha-reductase activity, this represents a highly efficient compensatory mechanism for androgen and estrogen production after puberty.
5-AD is worse than a waste, it is counterproductive unless you are a transexual. - Brock