[h=2]<h1>Testosterone - LH and FSH. ATD (3,17-dioxo-etiochol-1,4,6-triene)</h1>
S.A.R.M. Site Specific Androgen Receptor Modulation – Get Big, Stay Big[/h]
S.A.R.M. Site Specific Androgen Receptor Modulation – Get Big, Stay Big[/h]
Recently many readers have been writing in asking questions about how to use one of the hottest new supplements to hit the market – ATD (3,17-dioxo-etiochol-1,4,6-triene). ATD is possibly the greatest recent supplement breakthrough allowing for tremendous natural testosterone production and HPTA up-regulation. And no, I’m not talking about another “tribulus” or “deer antler velvet” supplement. ATD also has some unique properties that are of great interest to bodybuilders. To fully appreciate this amazing compound, a short review of HPTA regulation is in order.
Primer:
There are two primary negative feedback mechanisms involved in male testosterone production.
1) Elevated estrogen levels due to aromatase activity acts upon the hypothalamus decreasing GnRH production.
2) Elevated androgen levels directly stimulate androgen receptors on the hypothalamus resulting in decreased GnRH production.
Decreased GnRH production reduces LH and FSH production, which are directly involved in the production of testosterone.
Until recently, most post-cycle recovery protocols have focused on two aspects of HPTA regeneration.
1) Estrogen control (either through aromatase inhibition or a S.E.R.M. (Selective Estrogen Receptor Modulator) such as tamoxifen or clomephine.
2) Direct stimulation of testosterone production using HCG (by mimicking LH) or clomephine, which seems to directly stimulate LH production.
The first aspect of this approach is highly effective. High-normal testosterone levels can be achieved post-cycle using estrogen control alone. The second approach doesn’t actually restore HPTA function, but does have positive effects in maintaining testicular function prior to HPTA regeneration.
The above approach neglects a significant piece of HPTA regulation and inhibition; androgenic stimulation of the hypothalamus. ATD addresses the androgenic feedback mechanism. Technically, you could call ATD a Selective Androgen Receptor Modulator (S.A.R.M.). Yup, you guessed it. This is kind of like tamoxifen but on the other side of the equation. ATD has 90% androgenic activity in muscle tissue but only 10% androgenic activity in the hypothalamus.
Most will recall that tamoxifen blocks estrogen receptors in breast tissue, but has positive estrogenic effects in other tissues (i.e. liver, bone etc.). Similarly, ATD site-specifically blocks androgen activity exactly where we want it – in the hypothalamus. As your body produces more and more testosterone, ATD tricks your hypothalamus into thinking your testosterone levels are low.
But won’t the anti-androgen activity interfere with muscle growth? Recall ATD has 90% androgenic activity in muscle cells. This is insignificant when you consider that your body is now producing testosterone equivalent to injecting 400-600mg per week of testosterone enanthate or cypionate.
This has several very interesting implications. First of all, when estrogen control is employed through an AAS protocol, benefits can include increased hardness, lower blood pressure, and decreased female fat deposits (including gyno). But while some may believe that co-administration of AAS and anti-estrogens reduce HPTA inhibition, this is only true in protocols involving low-androgenic anabolics, which typically have less inhibition anyway. The reason for this is because of the androgenic over stimulation in the hypothalamus, driving the androgen based negative feedback loop.
Oh, and by the way, I should also mention that ATD also causes significant aromatase inhibition.
Now we have another tool in our belt to consider—ATD. By controlling the androgen feedback loop, a world of possibilities opens up.
Natural Performance Enhancement
The truth is, a man’s testicles are capable of creating quite a lot of testosterone. By naturally controlling the negative feedback mechanisms, significant increases in natural testosterone production are possible. For healthy non-hypogonadal males, increases of testosterone up to 400% have been seen while using Ultra H.O.T. For the natural athlete this means continued growth and progress without the typical problems associated with exogenous testosterone use. Also, because the body is naturally producing the extra testosterone, the athlete’s testosterone-epitestosterone ratio stays within the normal range.
Post-cycle Recovery
Earlier, I discussed the use of various pharmaceuticals to speed the recovery of natural testosterone production post-cycle. While quite effective, there’s a better, more cost-effective approach. Because ATD is a hypothalamus-specific anti-androgen, testosterone production resumes faster and stronger.
Usually, it doesn’t make sense to start post-cycle recovery until androgens have cleared the system. This is because money is simply wasted due to the overriding effect of the androgen negative feedback loop. However, with ATD benefits can be realized even when longer acting esters have not completely cleared the system. This addresses the post-cycle therapy timing problems associated with longer acting esters.
One note: Much of the HPTA suppression from trenbolone and nandrolone is from progesterone receptor activity. ATD is highly effective once these compounds have cleared the system, however it does not counter the progesterone receptor activity. (I’ll come back to this thought.)
More Muscle / Bigger Balls
As mentioned before, some have co-administered estrogen control during an AAS cycle in a failed attempt to reduce HPTA inhibition. Now for the exciting part. Consider this real-world test recently performed in Mexico.
16 test subjects were monitored to observe the interaction between ATD and methyl testosterone compared to anastrozole and methyl testosterone, ATD only and placebo. ALRI’s Ultra H.O.T. contains ATD and was used for this test.
1) Four were given a placebo.
2) Four were given an ATD analog once daily. (4 capsules of Ultra H.O.T.)
3) Four were given 100mg methyl testosterone/1.5mg anastrozole daily.
4) Four were given 100mg methyl testosterone/ATD analog once daily. (4 capsules of Ultra H.O.T.)
1) Obviously the first four realized no significant changes in LH/FSH/estradiol/testosterone at two, four and eight week retesting periods
2) The ATD analog only group showed an average 50% decrease in estradiol, and a significant increase in LH/FSH/testosterone.
3) The anastrazol/methyl testosterone group all showed a significant increase in testosterone (gee, are you surprised?) and a descending decrease in LH/FSH over the eight week period until near zero, and estradiol levels increased an average of 1.6 times normal.
4) The ATD analog/Methyltestosterone group of course had a major increase in testosterone. LH/FSH decreased after the first two weeks an average of 34% but remained constant until termination of the project at week eight. Estradiol was an average of 1.9 times normal.
Co-administration of ATD and AAS seems to maintain significant testicular function even after eight weeks of continuous use. Again, this test was performed using methyltestosterone. In theory, nandrolone and trenbolone would still cause significant inhibition due to progesterone receptor activity. But what if you want to have your cake and eat it too?
ALRI has recently come out with Max LMG. Max LMG is a progesterone derivative with anti-progesterone properties. It stands to reason that co-administering nandrolone, Max LMG and Ultra H.O.T. would produce very favorable results with minimal inhibition. (If one lived in a freethinking country where such things were permitted) However, I do not have any personal experience to validate this.
Bridging the Gap
Low-dose bridges are often misunderstood. Without controlling the androgen side of the HPTA feedback mechanism, bridging is strictly counter-productive. Any exogenous androgen administration simply reduces the amount of testosterone naturally produced post-cycle. Technically, one could use ATD co- administered with low-dose AAS successfully as a bridge. Unlike normal “bridge” cycles, ATD addresses the both the androgen feedback loop and the estrogen feedback loop. In fact, recent Mexican test subjects experienced no inhibition even while co-administering 250mg per week of testosterone enanthate.
Keep in mind that natural athletes have experienced significant up-regulation in testosterone production with ATD alone. Hopefully you see that while bridging with ATD works, it’s really not necessary
Putting it all Together:
Controlling both the androgen and estrogen modes of HPTA inhibition leaves many more options available to an athlete. Using any of the above applications will allow an athlete to experience continued progress without disappointing significant others. That’s right guys, make great gains and leave the potato at home!
Currently there are very few products I am aware of containing ATD. Whichever brand you choose, be aware that taking the correct dose is key. My own bias of course is ALRI’s Ultra H.O.T, which contains ATD plus other natural aromatase inhibitors and estrogen clearing compounds.
By Author L. Rea
Primer:
There are two primary negative feedback mechanisms involved in male testosterone production.
1) Elevated estrogen levels due to aromatase activity acts upon the hypothalamus decreasing GnRH production.
2) Elevated androgen levels directly stimulate androgen receptors on the hypothalamus resulting in decreased GnRH production.
Decreased GnRH production reduces LH and FSH production, which are directly involved in the production of testosterone.
Until recently, most post-cycle recovery protocols have focused on two aspects of HPTA regeneration.
1) Estrogen control (either through aromatase inhibition or a S.E.R.M. (Selective Estrogen Receptor Modulator) such as tamoxifen or clomephine.
2) Direct stimulation of testosterone production using HCG (by mimicking LH) or clomephine, which seems to directly stimulate LH production.
The first aspect of this approach is highly effective. High-normal testosterone levels can be achieved post-cycle using estrogen control alone. The second approach doesn’t actually restore HPTA function, but does have positive effects in maintaining testicular function prior to HPTA regeneration.
The above approach neglects a significant piece of HPTA regulation and inhibition; androgenic stimulation of the hypothalamus. ATD addresses the androgenic feedback mechanism. Technically, you could call ATD a Selective Androgen Receptor Modulator (S.A.R.M.). Yup, you guessed it. This is kind of like tamoxifen but on the other side of the equation. ATD has 90% androgenic activity in muscle tissue but only 10% androgenic activity in the hypothalamus.
Most will recall that tamoxifen blocks estrogen receptors in breast tissue, but has positive estrogenic effects in other tissues (i.e. liver, bone etc.). Similarly, ATD site-specifically blocks androgen activity exactly where we want it – in the hypothalamus. As your body produces more and more testosterone, ATD tricks your hypothalamus into thinking your testosterone levels are low.
But won’t the anti-androgen activity interfere with muscle growth? Recall ATD has 90% androgenic activity in muscle cells. This is insignificant when you consider that your body is now producing testosterone equivalent to injecting 400-600mg per week of testosterone enanthate or cypionate.
This has several very interesting implications. First of all, when estrogen control is employed through an AAS protocol, benefits can include increased hardness, lower blood pressure, and decreased female fat deposits (including gyno). But while some may believe that co-administration of AAS and anti-estrogens reduce HPTA inhibition, this is only true in protocols involving low-androgenic anabolics, which typically have less inhibition anyway. The reason for this is because of the androgenic over stimulation in the hypothalamus, driving the androgen based negative feedback loop.
Oh, and by the way, I should also mention that ATD also causes significant aromatase inhibition.
Now we have another tool in our belt to consider—ATD. By controlling the androgen feedback loop, a world of possibilities opens up.
Natural Performance Enhancement
The truth is, a man’s testicles are capable of creating quite a lot of testosterone. By naturally controlling the negative feedback mechanisms, significant increases in natural testosterone production are possible. For healthy non-hypogonadal males, increases of testosterone up to 400% have been seen while using Ultra H.O.T. For the natural athlete this means continued growth and progress without the typical problems associated with exogenous testosterone use. Also, because the body is naturally producing the extra testosterone, the athlete’s testosterone-epitestosterone ratio stays within the normal range.
Post-cycle Recovery
Earlier, I discussed the use of various pharmaceuticals to speed the recovery of natural testosterone production post-cycle. While quite effective, there’s a better, more cost-effective approach. Because ATD is a hypothalamus-specific anti-androgen, testosterone production resumes faster and stronger.
Usually, it doesn’t make sense to start post-cycle recovery until androgens have cleared the system. This is because money is simply wasted due to the overriding effect of the androgen negative feedback loop. However, with ATD benefits can be realized even when longer acting esters have not completely cleared the system. This addresses the post-cycle therapy timing problems associated with longer acting esters.
One note: Much of the HPTA suppression from trenbolone and nandrolone is from progesterone receptor activity. ATD is highly effective once these compounds have cleared the system, however it does not counter the progesterone receptor activity. (I’ll come back to this thought.)
More Muscle / Bigger Balls
As mentioned before, some have co-administered estrogen control during an AAS cycle in a failed attempt to reduce HPTA inhibition. Now for the exciting part. Consider this real-world test recently performed in Mexico.
16 test subjects were monitored to observe the interaction between ATD and methyl testosterone compared to anastrozole and methyl testosterone, ATD only and placebo. ALRI’s Ultra H.O.T. contains ATD and was used for this test.
1) Four were given a placebo.
2) Four were given an ATD analog once daily. (4 capsules of Ultra H.O.T.)
3) Four were given 100mg methyl testosterone/1.5mg anastrozole daily.
4) Four were given 100mg methyl testosterone/ATD analog once daily. (4 capsules of Ultra H.O.T.)
1) Obviously the first four realized no significant changes in LH/FSH/estradiol/testosterone at two, four and eight week retesting periods
2) The ATD analog only group showed an average 50% decrease in estradiol, and a significant increase in LH/FSH/testosterone.
3) The anastrazol/methyl testosterone group all showed a significant increase in testosterone (gee, are you surprised?) and a descending decrease in LH/FSH over the eight week period until near zero, and estradiol levels increased an average of 1.6 times normal.
4) The ATD analog/Methyltestosterone group of course had a major increase in testosterone. LH/FSH decreased after the first two weeks an average of 34% but remained constant until termination of the project at week eight. Estradiol was an average of 1.9 times normal.
Co-administration of ATD and AAS seems to maintain significant testicular function even after eight weeks of continuous use. Again, this test was performed using methyltestosterone. In theory, nandrolone and trenbolone would still cause significant inhibition due to progesterone receptor activity. But what if you want to have your cake and eat it too?
ALRI has recently come out with Max LMG. Max LMG is a progesterone derivative with anti-progesterone properties. It stands to reason that co-administering nandrolone, Max LMG and Ultra H.O.T. would produce very favorable results with minimal inhibition. (If one lived in a freethinking country where such things were permitted) However, I do not have any personal experience to validate this.
Bridging the Gap
Low-dose bridges are often misunderstood. Without controlling the androgen side of the HPTA feedback mechanism, bridging is strictly counter-productive. Any exogenous androgen administration simply reduces the amount of testosterone naturally produced post-cycle. Technically, one could use ATD co- administered with low-dose AAS successfully as a bridge. Unlike normal “bridge” cycles, ATD addresses the both the androgen feedback loop and the estrogen feedback loop. In fact, recent Mexican test subjects experienced no inhibition even while co-administering 250mg per week of testosterone enanthate.
Keep in mind that natural athletes have experienced significant up-regulation in testosterone production with ATD alone. Hopefully you see that while bridging with ATD works, it’s really not necessary
Putting it all Together:
Controlling both the androgen and estrogen modes of HPTA inhibition leaves many more options available to an athlete. Using any of the above applications will allow an athlete to experience continued progress without disappointing significant others. That’s right guys, make great gains and leave the potato at home!
Currently there are very few products I am aware of containing ATD. Whichever brand you choose, be aware that taking the correct dose is key. My own bias of course is ALRI’s Ultra H.O.T, which contains ATD plus other natural aromatase inhibitors and estrogen clearing compounds.
By Author L. Rea
