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ATD is it useless afterall?
- Thread starter AX_Ryan
- Start date
macrophage69alpha
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AX_Ryan said:
then that is quite unfortunate.
Triple J
New member
Just to be clear I was not trying to start, or get in the middle of a pissing contest but I did want to learn more about my ATD results which were not as expected, and miserable in comparison to other estrogen suppression products I have used. Without any firm data one can only speculate if the product was suppressing too much estrogen, or if the issue was complicated by androgen receptor blocking as Ryan's data indicate a possibilty. I do believe there was something detrimental going on beyond estrogen suppression. It looks like the jury is still out on this issue but in my clinical setting the verdict is in.
My theory on progestins may apply to this product. Younger bros with plenty of AR's are not as often affected negatively by progestins, in terms of the dreaded "deca dick". As one gets older you lose ARs. At some point you lose enough ARs that your system becomes more delicate, and competitive inhibition from other AR lockers (like deca - 2x as strong affinty for the AR as T) can block that DHT signal to your dick, and you get deca dick. Thus the advice to always run the T with the deca, or even 2x or more the deca. For some even this will not help any longer. Another factor is when androgen reception is blocked dopamine is inhibited, prolactin goes up, etc.
Since I was probably one of the older bros running this ATD product, and I was running it natural, I was more susceptable to any androgen blocking effects. Cause everything I experienced while on the ATD was like a mini "crash" post-cycle. I got off it before my physique or work-outs were were effected too much. I am not back to normal yet but seem to be recovering.
My theory on progestins may apply to this product. Younger bros with plenty of AR's are not as often affected negatively by progestins, in terms of the dreaded "deca dick". As one gets older you lose ARs. At some point you lose enough ARs that your system becomes more delicate, and competitive inhibition from other AR lockers (like deca - 2x as strong affinty for the AR as T) can block that DHT signal to your dick, and you get deca dick. Thus the advice to always run the T with the deca, or even 2x or more the deca. For some even this will not help any longer. Another factor is when androgen reception is blocked dopamine is inhibited, prolactin goes up, etc.
Since I was probably one of the older bros running this ATD product, and I was running it natural, I was more susceptable to any androgen blocking effects. Cause everything I experienced while on the ATD was like a mini "crash" post-cycle. I got off it before my physique or work-outs were were effected too much. I am not back to normal yet but seem to be recovering.
Last edited:
Goldprospector
New member
First of all, props to both Ryan and Macro for a very good debate on issues regarding supps that are used by the BBing comunity. This was handled on a very professional manner.
It is great to see this kind of thread going on. Not because of any selling wars or product boosting, but just to show the research of the products and knowledge of the manufacturers.
Tanks again guys, K for both!
It is great to see this kind of thread going on. Not because of any selling wars or product boosting, but just to show the research of the products and knowledge of the manufacturers.
Tanks again guys, K for both!
macrophage69alpha
New member
all steroidal ai's bind to the AR, very weakly
6-Methylenandrosta-1,4-diene-3,17-dione (FCE 24304): a new irreversible aromatase inhibitor.
Giudici D, Ornati G, Briatico G, Buzzetti F, Lombardi P, di Salle E.
Farmitalia C. Erba, R.&D./Oncology, Nerviano (MI), Italy.
FCE 24304 (6-methylenandrosta-1,4-diene-3,17-dione), a new irreversible aromatase inhibitor, has been identified and characterized in vitro and in vivo. The compound caused time-dependent inactivation of human placental aromatase with a t1/2 of 13.9 min and ki of 26 nM. When tested in PMSG-treated rats, ovarian aromatase activity was reduced 24 h after dosing by both the s.c. (ED50 1.8 mg/kg) and the oral (ED50 3.7 mg/kg) routes. No interference with 5 alpha-reductase activity nor any significant binding affinity for estrogen receptor was found. Slight binding affinity for the androgen receptor (RBA 0.2% of DHT) was observed.
6-Methylenandrosta-1,4-diene-3,17-dione (FCE 24304): a new irreversible aromatase inhibitor.
Giudici D, Ornati G, Briatico G, Buzzetti F, Lombardi P, di Salle E.
Farmitalia C. Erba, R.&D./Oncology, Nerviano (MI), Italy.
FCE 24304 (6-methylenandrosta-1,4-diene-3,17-dione), a new irreversible aromatase inhibitor, has been identified and characterized in vitro and in vivo. The compound caused time-dependent inactivation of human placental aromatase with a t1/2 of 13.9 min and ki of 26 nM. When tested in PMSG-treated rats, ovarian aromatase activity was reduced 24 h after dosing by both the s.c. (ED50 1.8 mg/kg) and the oral (ED50 3.7 mg/kg) routes. No interference with 5 alpha-reductase activity nor any significant binding affinity for estrogen receptor was found. Slight binding affinity for the androgen receptor (RBA 0.2% of DHT) was observed.
macrophage69alpha
New member
J Clin Endocrinol Metab. 1984 Dec;59(6):1088-96. Related Articles, Links
Inhibition of aromatization stimulates luteinizing hormone and testosterone secretion in adult male rhesus monkeys.
Ellinwood WE, Hess DL, Roselli CE, Spies HG, Resko JA.
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.
btw- its funny how the data from this study has been misintepreted with respect to the 17hydroxyl metabolite (the one mentioned in the ALRI- now AX- sales pitch)
Inhibition of aromatization stimulates luteinizing hormone and testosterone secretion in adult male rhesus monkeys.
Ellinwood WE, Hess DL, Roselli CE, Spies HG, Resko JA.
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.
btw- its funny how the data from this study has been misintepreted with respect to the 17hydroxyl metabolite (the one mentioned in the ALRI- now AX- sales pitch)
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