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E-CONTROL Rx™ - Anti-Estrogen

IronMagLabs

IronMagLabs

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E-CONTROL Rx™ - Anti-Estrogen

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- Decreases Estrogen
- Increases Testosterone
- Effective for PCT (Post Cycle Therapy)

1,4,6-Androstatriene-3,17-dione is a potent irreversible aromatase inhibitor. It inhibits estrogen biosynthesis by permanently binding and inactivating aromatase in adipose and peripheral tissue. By reducing the production of estrogen, circulating estrogen levels drop which in turn indirectly increases testosterone levels.

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1,4,6 Androstatriene-dione (ATD)

Characteristics

ATD is a steroidal aromatase inhibitor, known as a suicidal inhibitor because it permanently binds to the aromatase enzyme.

ATD is used for its aromatase inhibiting and testosterone boosting effect. Its effectiveness at lowering estrogen appears to be stronger than 6-oxo. It converts to 1,4,6-testosterone, which would also be expected to cause falsely high readings for a testosterone analysis.

The 1,4,6-testosterone metabolite of ATD can also bind to the androgen receptor (AR) and induce androgenic (or possibly anti-androgenic) effects similar to what is seen from 6-oxo. This would be expected since 1,4,6-testosterone has about one third the binding affinity for the AR, therefore it may interefere with the anabolic or androgenic action of hormones which bind the androgen receptor.

ATD would also be expected to interfere with production of natural testosterone by acting upon the hypothalamus pituitary testicular axis (HPTA), therefore this compound should not be used during post cycle therapy (PCT), however it could successfully be used during a cycle to help keep estrogen in control. Anecdotal reports and animal studies have also shown ATD inhibits libido and general sexual potency.

References

Effect of an inhibitor of aromatization, 1,4,6 androstatriene-3,17-dione (ATD) on LH release and steroid binding in hypothalamus of adult female rats.

Exp Brain Res. 1986;64(3):407-10.
Slama A, Gogan F, Sarrieau A, Vial M, Rostene W, Kordon C.

Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis.
ME Kaplan and MY McGinnis
Horm Behav, Mar 1989; 23(1): 10-26.

Anabolic Pharmacology
Seth Roberts (2009)

By Jason Rowland

Chemical Name(s):

Androsta-1,4,6-triene-3,17-dione
1,4,6-androstatriene-3,17-dione
Chemical Formula: C19H22O2
Molecular Weight: 282
CAS: NA
Q Qatio: NA
Anabolic #: NA
Androgenic #: NA
Oral Bioavailability: Estimated at 4%
AR Binding Affinity: NA
SHBG Binding Affinity: NA
Half Life: 2 days
Legal Status (US): Not listed as a controlled substance
Average Dose: 25-100mg/day
Average Cycle Length: 4-8 weeks
 

Attachments

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J Clin Endocrinol Metab. 1984 Dec;59(6):1088-96.

Inhibition of aromatization stimulates luteinizing hormone and testosterone secretion in adult male rhesus monkeys.

Ellinwood WE, Hess DL, Roselli CE, Spies HG, Resko JA.

Abstract

Experiments were conducted to examine the role of aromatization in the control of LH and testosterone secretion in adult male rhesus monkeys. Treatment of male monkeys (n = 7) with sc Silastic packets containing the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) resulted in 1.5- to 3-fold elevations in serum LH and testosterone concentrations in six of seven animals. Concurrent treatment of ATD-treated monkeys with small quantities of estradiol-17 beta (n = 4) abolished the stimulatory effect of ATD. During ATD treatment, peripheral estradiol levels were reduced by 30% and hypothalamic aromatase activity, as determined in vitro, was reduced 80-90%. The lack of androgenic or antiandrogenic activity of ATD was demonstrated by its inactivity in either a mouse seminal vesicle bioassay or a highly sensitive penile spine bioassay. Furthermore, ATD did not react with rat prostatic or hypothalamic cytosol androgen receptors. 1,4,6-Androstatriene-17-ol-3-one, a possible metabolite of ATD in vivo, did react with prostatic and hypothalamic androgen receptors, but possessed no antiandrogenic activity in either bioassay. Thus, treatment of adult males with an aromatase inhibitor that inhibits both peripheral and central aromatization, and which has no apparent antiandrogenic activity, results in stimulation of LH and testosterone secretion. These data demonstrate that aromatization of androgens to estrogens plays an important role in negative feedback regulation of LH secretion and maintenance of normal testosterone levels in adult male primates.


PMID: 6541658 [PubMed - indexed for MEDLINE]
 
ATD for Estrogen Control & PCT

ATD (3,17-dioxo-etiochol-1,4,6-triene) is a recent introduction to estrogen control. It is thought to stop estrogen production in a manner similar to steroidal AI’s such as exemestane. Brand name ATD’s are Rebound XT, Rebound Reloaded, Novedex XT, Ultra H.O.T and Ultra H.O.T.ter.

ATD is technically an aromatase inhibitor, but with some interesting properties that make it a very useful addition to our estrogen control arsenals.

There are two negative feedback loops that we try to correct through post cycle therapy. The first is elevated estrogen levels from aromatase activity act on the hypothalamus to decrease GnRH production. The second is that elevated androgen levels stimulate androgen receptors in the hypothalamus causing decreased GnRH production. Decreased GnRH leads to reduced LH and FSH production, both of which are directly involved in testosterone production.

Typical PCT with SERM’s and AI’s address the estrogen component of this negative feedback, but do nothing for androgenic stimulation of the hypothalamus. ATD addresses the androgenic feedback loop. ATD has 90% androgenic activity in muscle tissue but only 10% androgenic activity in the hypothalamus.

ATD works for androgen activity the same way that tamoxifen works for estrogen. Tamoxifen blocks estrogen in breast tissue, but has positive effects in other tissue such as liver and bone. ATD blocks androgens in the hypothalamus, but allows it to be active in other tissue.

Because of this dual action estrogen levels are lowered while testosterone levels begin to rise. This is because ATD tricks your hypothalamus into thinking testosterone levels are low so it produces more. ATD provides benefits far beyond simply controlling estrogen in your body. Through its control over the androgen negative feedback loop testosterone production is restarted much faster. And the faster you recover your natural testosterone production the easier it is to keep muscular gains.
In addition to ATD’s benefits for post cycle therapy studies have shown that employing ATD during AAS use maintains significant HPTA function. This means reduced testicular atrophy and faster post-cycle recovery. This is something that you simply can’t get from estrogen control alone.

ATD can also be used by the natural athlete to increase testosterone production. In studies increases of up to 400% in testosterone have been seen. This is equivalent to injecting 400-600mg per week of testosterone enanthate or cypionate. This means continued growth for the natural athlete without the problems and side effects usually associated with injecting testosterone.

While there should technically not be any difference between the ATD ptoducts I have personally seen the best results using Rebound XT by Designer Supplements. I believe it is also the most cost effective of the ATD products out there. Your mileage may vary.

I’ve found the following discussion on running SERM’s inverse to ATD’s which is both informative and by all accounts very effective. It has been posted on many forums and the credit for it goes to Dr. D. Thank you Dr. D!
“Discussion on running SERM inverse to ATD.

Estrogen only “rebounds” based on the mechanism of suppression. SERM, for example, only masks estrogen expression by occupying receptors but estrogen production is left unchecked and actually increases as testosterone levels increase. AI’s like letro inhibit inducible enzymes and just like a leaky faucet, they body will eventually try to balance the equation with increased aromatase activity. Steroidal AI’s like Teslac, Exemestane, and ReboundXT will not result in ‘rebound’ phenomena because the inhibition is non-competitive and irreversible. They act as false substrates, so aromatase is still happy to act on them (instead of androstenedione) and the body keeps no record of an imbalance. There is no leaky faucet. In fact, after prolonged use, steroidal AI’s often produce a protracted anti-e benefit even after being discontinued. This is why I suggest an inverse taper with SERM and RXT for PCT with an abrupt stoppage of RXT at the end. As the SERM elevates androgen/estrogen production, the AI dose is increased to compensate while the SERM is phased out. It works quite well to use this approach and rebound is not encountered. Adding LX and/or DHEA also really makes for a killer PCT in this scheme.

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