ultra hot

[wastedwhiteboy2]

there has been some discussion about when to use this product. I'd like to hear whether or not this should be used pct and why?

I have a bottle I was just thinking of waiting til after pct to start it.

 

[Mr.50]

I think ALRI has already said that it would be good for PCT. The question not answered is whether or not itt will have any beneficial effect during a cycle at keeping the hypothalamus/pituitary from sensing that there is excess androgens in the body?


Mr.50

 

[Alpha Dog]

I agree. It should be good for PCT. It defiantly contains some good suicide inhibitors. I don't doubt that it will increase T post cycle.

As Mr. 50 points out, whether it truly is an effective AR agonist centrally and not peripherally is another question altogether. With regards to this question, if the good folks at ALRI would be so kind as to take a gander at this thread, I would be grateful.

http://anabolicminds.com/forum/showthread.php?t=27487

 

[wastedwhiteboy2]

ok the anti estrogen effects would help with the pct. but, would it be any better than nolva or any other anti estrogen. or would it be more beneficial to run it after pct. it sounds like it stops the body from detecting extra testosterone and lets you get to high levels. I think I'm leaning more towards activate to add to nolva for pct.

 

[Alpha Dog]

ok the anti estrogen effects would help with the pct. but, would it be any better than nolva or any other anti estrogen.

Well, nolva is not technically an anti-estrogen. It is an estrogen receptor antagonist. For that matter, I am not a advocate of running high doses of anti-e's and estrogen receptor antagonists concurently post cycle. So, if you have nolva on hand, I wouldn't bother.

Would it be better than another anti-estrogen, like Androstenetrione (6-OXO)? Interesting question. When I was researching ATD, I found that PA actually references it in his 6-OXO writeup. Check out the third referenece here

ATD is 1,4,6-androstatriene-3,17-dione. So, why didn't he use it? He must have looked at it if it is included in one of the studies he references. Authur must have seen something in it that PA didn't. So, I guess we'll just have to wait and see to find out if it is better than the other anti-e's on the market.

 

[Author L. Rea]

Bow:

I just got back to the US lastnight and have taken a few minutes to read some of your posts with rather red eyes. Have to say that it is good to see people are thinking and that I enjoyed your thoughts a great deal.

Hmmm, so can an anti-androgen work site-secifically (hypothalamic AR) yet allow the action of circulatory androgens to do their thing peripherally seems to be the topic of interest here.

Let's start with is it really all that difficult to believe? After all we are all well aware that Nolvadex is far more effective at binding to ER in the breast tissue yet has a bell-curve value in other tissues. It is all about affinity as a whole.

There have been some excellent studies in this regard applying to the androgen modulation values of ATD analogs (we have a multiple patents pending on several at this time for this purpose) that you may wish to review.

1) Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis. Kaplan ME, McGinnis MY. Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.
2) 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.
3) J Steroid Biochem. 1986 Oct;25(4):593-600. Effect of 1,4,6-androstatriene-3,17-dione (ATD), 4-hydroxy-4- androstene-3,17-dione (4-OH-A) and 4-acetoxy-4-androstene-3,17-dione (4-Ac-A) on the 5 alpha-reduction

The studies supported a belief I had spoken of in past articles and books in regard to the tissue-specific affinity possesed by some compounds similar to the way that DHT has a higher affinity for sex specific tissues than for peripheral tissues. This "suggested" the ability to either trigger or inhibit an action in specific tissues of ones choosing to a significant extent.

This was further inspired by my friend Bruce Kneller in regard to his research on ATD as a hypothamic aromatase inhibitor. (Amazingly bright lad!)

To put this belief to the real world test, we used 16 trained test subjects. (Done last year in Mexico)

1) 4 were given a placebo
2) 4 were given an ATD analog daily
3) 4 were given 100mg methyl testosterone/1.5mg anastrolzol daily
4) 4 were given 100mg methyl testosterone/ATD analog daily.

1) Obviously the first 4 realized no significant changes in LH/FSH/estradiol/testosterone at 2, 4 and 8 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 anastrolzol/methyl testosterone group all showed a significant increase in testosterone (gee, are you surprised?) and a decending decrease in LH/FSH over the 8 week period until near 0, 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 2 weeks an average of 34% but remained constant until termination of the project at week 8. Estradiol was an average of 1.9 times normal.

What does this mean? Well, if in the latter two groups estradiol were near the same then the estrogen negative feed back loops were as well. However the continued endogenous (made in the body) production of LH/FSH STRONGLY suggests that the findings in the research above is applicable in that the androgen negative feed back loop was inhibited by the ATD analog.

There is a write up on these compounds coming out in my column in Planet Muscle mag this issue that is reasonably informative. I will likely post it after the issue has run its period.

I hope that helps to answer some questions and gives cause for thought.

Thank you;
ALR

 

[Knowbull]

ALR, thanks for your informative post. I appreciate it and look forward to more expositions regarding ALRI products, their uses, applications, benefits. Welcome to this board!

 

[Alpha Dog]

4) The ATD analog/Methyltestosterone group of course had a major increase in testosterone. LH/FSH decreased after the first 2 weeks an average of 34% but remained constant until termination of the project at week 8. Estradiol was an average of 1.9 times normal.

What does this mean? Well, if in the latter two groups estradiol were near the same then the estrogen negative feed back loops were as well. However the continued endogenous (made in the body) production of LH/FSH STRONGLY suggests that the findings in the research above is applicable in that the androgen negative feed back loop was inhibited by the ATD analog.

Wow. Only a 34% reduction after two weeks and then it remained constant. That is impressive. Especially considering the increase in estrogen. Estrogen exerts its negative effects on LH and FSH at the pitiuitary. So, if you adminster an anti-e along with ATD (or its analog), you have a very potent synergistic mix. I guess that's why you went with both an anti-e and an ATD analog in Ultra Hot. That is exactly the kind of data I was looking for.

Can you speculate as to whether its binding rate peripherally remained low? Anotherwords, in the fourth study, did the subjects experience increased anabolism somewhat consistent with what could be typically expected from 100 mg's methyl-T ed alone?

I hope that helps to answer some questions and gives cause for thought.

Thank you;
ALR

It helps tremendously. Thank you for your time. I can't believe you would even bother addressing this so promptly after what had to have been a great trip to Mexico. I will defiantly be playing with some new PCT protocols using Ultra Hot in the near future

 

[Author L. Rea]

In the study we saw no significant decrease in muscular anabolism in comparison. I do have to say that this is very likely dose dependent as in high enough (and seriously expensive) dosages the effect would be negative to some extent.

I also found it interesting that there was a reduction in hair loss commented upon by some who were test subjects. Please do not take this as conclusive (we have funded a dermatology study for hair loss as part on our patents but we need another 60 days to have some facts to work with) as it mean a hair savior for all. I personally think that it is a function of the decrease in sex-specific tissue estrogen production.

ALR

 

[jminis]

In the study we saw no significant decrease in muscular anabolism in comparison. I do have to say that this is very likely dose dependent as in high enough (and seriously expensive) dosages the effect would be negative to some extent.

I also found it interesting that there was a reduction in hair loss commented upon by some who were test subjects. Please do not take this as conclusive (we have funded a dermatology study for hair loss as part on our patents but we need another 60 days to have some facts to work with) as it mean a hair savior for all. I personally think that it is a function of the decrease in sex-specific tissue estrogen production.

ALR

ALR thanks for stopping bye with those studies. I have to say I'm still on the fence on where to incorporate this into my cycles. After reading BTPB I run those short phase cycles you discuss and I have to say I love them for all the obvious reasons.

So taking that into consideration would you say Ultra Hot would be better suited to run on cycle to make recovering that much easier or during PCT? If you want I've incorporated a link to my cycle outline I think you'd be proud, lol Oh and we have a very good mutual friend (he's lives in Florida, he's an NGA pro and thinks he's the mack daddy of Ft Lauderdale. LOL I think you know who I'm referring to.

I'm interested in your thoughts recovery is my main focus so anything that could make it easier and quicker I'm all for it.

http://www.anabolicminds.com/forum/showthread.php?t=19178

 

[CDB]

Thank you;
ALR

Welcome to the boards.

 

[Onslaught]

ALR, the studies for the ATD analogue seem convincing enough, but how do we know ATD will cause the same effects?

 

[wastedwhiteboy2]

thats basically my question also.

 

[Alpha Dog]

ATD is 1,4,6-androstatriene-3,17-dione. Ulta Hot contains 3,17-dioxo-etiochol-1,4,6-triene. I believe this is the analog he is referring too.

 

[Author L. Rea]

Bow:

I am beginning to think that I need to give you a job. Your post is correct and thank you.

The structural name is altered to include the analog we were most impressed with at the time. Naturally, we prefer to continue to change and improve any product we offer. As such this I believe most will find this product to always getting better.

As to the studies, they do include ATD itself as well as analogs in regard to effect. It is in part why we had to include 39 in our patents. We are now working on two sort of "Super-ATD" variants we hope to have ready by the next run.

Thus far I have noted that a protocol such as below works very well with very favorable blood work results for hormonal, lipid and organ function.

Week 1-6: Max LMG
Week 4-10: N'Gorge
Week 4-10: Ultra HOT

Thanks;
ALR

 

[Author L. Rea]

J:

In regard to your protocol your structure was sound. Thanks for thinking Lad.

Assuming one has legal means to do so, the protocol and timing factors apply enhanced or not.

We are working on a systemic and tissue specific anti-catabolic right now that ("if" the second set of subjects again confirm the studies and the first group's results) will help the enhanced athlete keep much more of the AAS gains, and the non-enhanced athlete make better ones. I prefer to wait until this next group finishes next week before I fully support the prior findings.

ALR

 

[jminis]

J:

In regard to your protocol your structure was sound. Thanks for thinking Lad.

Assuming one has legal means to do so, the protocol and timing factors apply enhanced or not.

We are working on a systemic and tissue specific anti-catabolic right now that ("if" the second set of subjects again confirm the studies and the first group's results) will help the enhanced athlete keep much more of the AAS gains, and the non-enhanced athlete make better ones. I prefer to wait until this next group finishes next week before I fully support the prior findings.

ALR

Sounds good, hopefully everything runs according to plan in the next trial because a product like that could really come in handy. Keep us updated for sure, take care, J

 

[milwood]

ALR--as stated, thanks much for your input here.

 

[Mr.50]

I am already getting excited about a product like that along with Sledge's Melting Point!!!!

What a combo!

J:

In regard to your protocol your structure was sound. Thanks for thinking Lad.

Assuming one has legal means to do so, the protocol and timing factors apply enhanced or not.

We are working on a systemic and tissue specific anti-catabolic right now that ("if" the second set of subjects again confirm the studies and the first group's results) will help the enhanced athlete keep much more of the AAS gains, and the non-enhanced athlete make better ones. I prefer to wait until this next group finishes next week before I fully support the prior findings.

ALR

 

[Bigfishy]

Ok guys im sorry if i missed this somewhere along the line but I can't tell if this product is theoretically suppose to minimize "shutdown" while on cycle, or if it is suppose to be used as PCT?

 

[wastedwhiteboy2]

kind of foggy to me too, but I got out of it to use it on cycle to prevent some shutdown.

 

[Mr.50]

Guys,

the sum of it is that it is very useful for both purposes. Now I have used it for PCT and I find it great never experienced testicle volume like this. I am going to start a cycle of Ergomax and Max LMG on Saturday and I will also take the ULTRA HOT throughout to see if it has any beneficial effects and into PCT (though many feel it would not be needed for this type of cycle)

Mr.50

 

[Guest]

Is he postulating that you can take an anti-estrogen or inhibitor on low levels of testosterone and still produce LH....Hmmmmm

 

[jminis]

Is he postulating that you can take an anti-estrogen or inhibitor on low levels of testosterone and still produce LH....Hmmmmm

LOL

 

[Mr.50]

Sounds a lot like the protocol USP posted a little while ago but with the addition od the androgen blocker

 

[Alpha Dog]

Guys,

the sum of it is that it is very useful for both purposes. Now I have used it for PCT and I find it great never experienced testicle volume like this. I am going to start a cycle of Ergomax and Max LMG on Saturday and I will also take the ULTRA HOT throughout to see if it has any beneficial effects and into PCT (though many feel it would not be needed for this type of cycle)

Mr.50

Exactally. A couple of added thoughts.

It looks like it could be the first supplement available that allows for bridging (although the term still scares the hell out of me) during PCT. Most of the studies I have seen compare both ATD and its analogs binding affinity (Authors study above with methyl-T) to testosterone. So, it wouldn't be a very good idea (at least until we see some more bloodwork from different androgens) to try to bridge with anything that has a higher binding affinity than test. For this purposes, I would think either test base or even better, hydroxy test (perhaps transdermal) at a few hundred mgs a week would very interesting (and then bloodwork of course).

Second, it looks like it may help to slow shutdown during a cycle or perhaps even prevent total shutdown on a mild/short cycle. Again, for it to prevent total shutdown, the same rules above apply with regards to binding affinity. Although bloodwork may prove that this atd analog has a stronger binding affinity than some of the "other" poplular androgens in use today.

This is going to be fun to watch in the coming months.

 

[nandi]

Is he postulating that you can take an anti-estrogen or inhibitor on low levels of testosterone and still produce LH....Hmmmmm

This is a decent analysis of the current model of how estrogen regulates feedback.

http://jcem.endojournals.org/cgi/content/full/86/6/2600


At relatively low physiological levels of testosterone, aromatization is the mediator of feedback inhibition (or the dominant one) at the pituitary level. But as can be seen in figure 3 at the hypothalamic level, DHT as well as E2 act in a negative feedback manner.

 

[Mr.50]

good article!:thumbsup:

 

[Bigfishy]

Well shucks, that study's been a long time in coming. Now i don't mean to be a pain in the ass but what is this ATD's fuction in both blocking suppresion on cycle and hpta recovery post cycle? What i got from it is that it makes your body think that your test level are at a normal level, preventing some suppresion while on cycle. Wouldn't this effect be undesired during PCT? Or am I totally off track here? (rugby player, not a Dr/biologist/chemist)

 

[CDB]

Well shucks, that study's been a long time in coming. Now i don't mean to be a pain in the ass but what is this ATD's fuction in both blocking suppresion on cycle and hpta recovery post cycle? What i got from it is that it makes your body think that your test level are at a normal level, preventing some suppresion while on cycle. Wouldn't this effect be undesired during PCT? Or am I totally off track here? (rugby player, not a Dr/biologist/chemist)

That's what I was thinking too. A 10% reduction of sensitivity in muscle and a 90% reduction in the hypothalumus is I believe what's claimed. During PCT the point is to increase your test levels by blocking the activity of estrogen or blocking it's production outright. So I guess the question would be can it block a reaction to high testosterone but also not block a reaction to what your body perceives as low estrogen levels. And as someone already pointed out there are other hormones involved in a regulatory role here depending on the relative levels involved. It's pretty complex, and I'm honestly hoping someone comes along with a good plain English answer, as this is giving me a headache. I've searched PubMed and Scirus and haven't found a thing.

 

[Nate Dawg]

So what I got from the article was that you can run a low dose of testosterone, and with the addition of a strong AI such as arimidex, shutdown of endogenous testosterone production, LH and FSH pulses will be prevented or slowed down for some time even with the administration of exogenous testosterone. The reason the endo test production, LH/FSH pulses arent affected is because the arimidex is strong enough to prevent aromatization of the exogenous testosterone, and the adex actually lowers the levels of estradiol in the blood. It is the excessive aromatization of testosterone into estrogen and higher levels of estradiol that will slow and eventually shut down the bodies natural pulses of LH/FSH, thus reducing the amount of endogenous testosterone being produced. Is this what its saying? lol

The KTCZ kind of confused me on what it did exactly, it seemed like it wasnt really beneficial for anything because from what I understood it raises estradiol levels and increased aromatase activity. The one good thing I found about it in the article was that it said that the KTCZ quickly returned LH/FSH pulses to normal....so I dont know exactly how it quickly returned the pulses to normal if it is actually increasing aromatization and estradiol levels...I think I am not understanding something here quite right.

Here is the take home point that I got from it. Take low doses of testosterone with the addition of a strong AI (arimidex) and the amount of time it takes to become shutdown will be increased, for a short period the endogenous production of testosterone is unaltered, as are the LH/FSH levels. So it seems to me, for an AAS user, when coming into pct, it could be beneficial to run a low dose of testosterone, say 150mg-200mg/week with the addition of arimidex in a dosage range of 1-2mg/day (although in the study they loaded the first day with 30mg and then maintained at 5mg/day...pretty high dose for adex, but it worked) and run the low dose testosterone + high dose AI for 3-4 weeks after ending the cycle and LH/FSH pulses will be able to return quicker in that 3-4 week timeframe, speeding up the production of endogenous testosterone. So the body is able to begin recovery in this time frame, while the individual is not "crashing" since they are still recieving 150-200mg/week of testosterone, making post cycle a much smoother transition and less depressing. Even for AAS users who do not want to cycle off using due to their seriousness of the sport, it seems as though when they have a break between contests/competitions, they could drop down to this testosterone+AI combo and run it for ~6-8 weeks while hopefully getting the testicles back into natural working order and recovering their endogenous production, while the addition of HCG during their heavy usage before cycling down to their recovery dosage could be very beneficial to their recovery of endo test production. I dont think that this would work in the sense of the "never ending cycle" there would definetly be permanent damage I would think after running an exogenous hormone for so long without a break. But say maybe a 1-2 year period of straight usage, with a few breaks in the middle using the low dosage, it may help one recover when completely coming off the AAS. One thing that should probably be kept in consideration, is that the tests were only run for 5 days, so further testing should be done before completely trusting you will recover endo test production on this protocol.

LOL, this is very similar to USPLabs protocol. I thought it looked like a good idea, as I thought it would make a smoother transition into pct as you would not go from having all this gear running through you, then 10 days later you dont have anything, and I thought it may be possible to slightly recover test levels when running a lower dose, but didnt have anything to back up what i thought, so I kept my mouth shut lol.

 

[Alpha Dog]

That's what I was thinking too. A 10% reduction of sensitivity in muscle and a 90% reduction in the hypothalumus is I believe what's claimed. During PCT the point is to increase your test levels by blocking the activity of estrogen or blocking it's production outright. So I guess the question would be can it block a reaction to high testosterone but also not block a reaction to what your body perceives as low estrogen levels. And as someone already pointed out there are other hormones involved in a regulatory role here depending on the relative levels involved. It's pretty complex, and I'm honestly hoping someone comes along with a good plain English answer, as this is giving me a headache. I've searched PubMed and Scirus and haven't found a thing.

Estrogen acts primarily at the pituitary. High levels can decrease sensitivity to GnRH. Prolonged low levesl can also decrease sensitivity to GnRH. The pituitary when sensitive to GnRH then produces LH and FSH (the former being critical to test production in the testies and the latter to sperm production). There are a number of other negative feedback mechanisms involved at the pituitary, but this is a very simple overview.

Testosterone acts primarily at the hypothalamous. Low levels (real or perceived) stimulate GnRH at the hypothalamous.

So, during PCT, test production is low (hence the purpose of pct). The hypothalamous then produces GnRH. The pituitary senses the rise in GnRH and produces LH and FSH. If estrogen is low it is sensitive to the GnRH and produces LH and FSH. Assuming the testies are sensitive to LH (leydig cells primarily), the body produces test.

Then the loop continues. If you didn't have some type of a AR receptor agonist, the hypothalamous would sense the increase in test and downregulate the GnRH pulses. But with the receptor agonist, it theoretically does not sense the inrease and continues the cycle, ultimately producing higher levels of test.

There are a tons of other feedback variables involves, but that is the short and sweet version. So, yes, a ATD or it anaog could be very benefical during PCT for increasing natural testosterone levels.

 

[Dwight Schrute]

Assuming the testies are sensitive to LH (leydig cells primarily), the body produces test.

BIG assumption, especially coming off a cycle.

 

[Alpha Dog]

BIG assumption, especially coming off a cycle.

Yes it is. Enter hcg.

 

[Dwight Schrute]

Well then the rest is kind of pointless if you are using HCG

 

[CDB]

There are a tons of other feedback variables involves, but that is the short and sweet version. So, yes, a ATD or it anaog could be very benefical during PCT for increasing natural testosterone levels.

Cool deal. If I'm reading you right this is because blocking the activity of testosterone at the hypothalumus doesn't mess with the pituatary gland's reaction to estrogen or GnRH, so 'tricking' the body into thinking you have low estrogen with a SERM or actually having low estrogen would still serve as a trigger for ramping up testosterone production.

I guess what makes this complicated is it's not one simple loop but more like several linked loops that work in tandem.

 

[nandi]

The KTCZ kind of confused me on what it did exactly, it seemed like it wasnt really beneficial for anything because from what I understood it raises estradiol levels and increased aromatase activity.

The KTCZ was used to suppress natural testosterone production so T could be added back in an a known, graded manner.

Note here that DHT from the added back testosterone is still acting to suppress the hypothalamic gonadotropin pulse generator. Normally GnRH and LH are released in both basal and pulsatile fashions. If the DHT is interfering with the pulsatile nature of GnRH release, it could suppress natural T production.

CDM, what was measured was pooled LH, not a graph of the frequency of release. The latter is just as important, or more so than the former, in determining T production.

But T production was not measured, only LH.

Quoting,

"According to this perspective, any purely androgenic effect of testosterone remaining in the face of anastrazole blockade and near-physiological testosterone addback (third mechanism listed above) was insufficient in the present setting to suppress mean daily LH production. This inference does not exclude possible inhibition of pulsatile LH secretion, which was not studied here. Indeed, LH pulse frequency can be increased by antiandrogens and decreased by pharmacological amounts of nonaromatizable androgens in healthy young men

 

[Funny Monkey]

Sounds like it woudl be great for pct but what about if you just want to boost your test levels would this do the trick?
What about taking this and throwing in some ActiVate from Sledge?

 

[Nate Dawg]

Sounds like it woudl be great for pct but what about if you just want to boost your test levels would this do the trick?
What about taking this and throwing in some ActiVate from Sledge?

bencozzy is keeping a cycle log of the Ultra HOT, so far he has had really good gains, not running it post cycle, just as a stand alone test booster, working really good for him.

 

[Funny Monkey]

Cool deal. If I'm reading you right this is because blocking the activity of testosterone at the hypothalumus doesn't mess with the pituatary gland's reaction to estrogen or GnRH, so 'tricking' the body into thinking you have low estrogen with a SERM or actually having low estrogen would still serve as a trigger for ramping up testosterone production.

I guess what makes this complicated is it's not one simple loop but more like several linked loops that work in tandem.

low estrogen alone might not do the trick. From what I have been reading your androgen feedback system plays a huge role in recovery how most of us have missed this issue I do not know. If you have a high or probably even normal level of dht in your body it can sense the dht and think that test is fine even if estrogen is low.

One thing I do not understand is libido it is somehow involved with dht. In a nutshell you can have low estrogen and feel fine have great sex drive and still have low test/LH/FSH

Feel free to corrct me anyone if I am wrong

 

[lifted]

One thing I do not understand is libido it is somehow involved with dht. In a nutshell you can have low estrogen and feel fine have great sex drive and still have low test/LH/FSH

Feel free to corrct me anyone if I am wrong

I know that when doing PCT with tamox, my libido is actually MUCH higher than while on actual test....this usually begins to taper off at about the 3rd week of PCT. Then for the next couple weeks, my libido is almost non-existant. This is when doing a cycle of test only and propionate being the ester.....interesting stuff.

 

[hrtguy]

Article discussion on using ATD

http://www.readthecore.com/200505/intern.htm

Considering this thread, thought this might be of interest.

It covers 4 different uses for using ATD.

 

[Grassroots082]

That was a really good read, thanks HRTGuy.

Co-administration of ATD and AAS seems to maintain significant testicular function even after eight weeks of continuous use

Employing ATD during AAS use maintains signifigant HPTA function. This means reduced testicular atrophy and a faster post - cycle recovery.

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- Ultra-Hot 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.

Basically, H.O.T. can pretty much be used while on cycle to maintain testicular function, post cycle to control estrogen and lead to a quicker recovery and after PCT as a bridge. DO I NEED TO CYCLE OFF?!?! :rofl: :drunk:

 

[hrtguy]

Do I need to Cycle off?

Grassroots,
It is recommended that every 4-8 weeks you cycle off for 4-8 weeks.

The reason is simple. After 8 weeks of continuous use, action-reaction factors in theory could make it less effective. Note: I don't know if long term use has actually been studied. (Perhaps ALR knows) We know that Foremstane remains quite effective for as long as 22 weeks continuous.

In fact, switching between Ultra H.O.T. and Formestane makes a lot of sense. Foremestane also actually decreases Estrogen and Progesterone receptor counts.

Of course, you could substitute foremstane for others as well.

 

[Grassroots082]

Grassroots,
It is recommended that every 4-8 weeks you cycle off for 4-8 weeks.

The reason is simple. After 8 weeks of continuous use, action-reaction factors in theory could make it less effective. Note: I don't know if long term use has actually been studied. (Perhaps ALR knows) We know that Foremstane remains quite effective for as long as 22 weeks continuous.

In fact, switching between Ultra H.O.T. and Formestane makes a lot of sense. Foremestane also actually decreases Estrogen and Progesterone receptor counts.

Of course, you could substitute foremstane for others as well.

Thanks HRTGuy, I was just being sarcastic, I wouldn't want to stay on any supp for that long and usually take breaks from all supplements for a couple weeks here and there. H.O.T definately sounds good though and look forward to giving it a run in the near future.

 

[Alpha Dog]

Two more questions:

1. I noticed that Ultra Hot includes 7beta-Hydroxy-DHEA. However, it is not mentioned in the writeup. Can you give us any indication of how much 7b-hyrdoxy-dhea is in the proprietary mix? Trying to get a grip on If I need to supplement with anything else (additional 7-oh, PS, etc) for cortisol control during PCT.

2. Any idea what the effects the two AI's (the ATD analog and 3-OHAT) are going to have on lipid profiles. I understand that most AI's are not beneficial in regards to restoring lipid profiles during PCT and this has been further demonstrated with Designer's Rebound (which also uses ATD as its AI). I ask being that I am trying to balance the dosing of Ultra-Hot with restoring my lipid profiles after a four week cycle which includes SD.

Thanks.

 

[Author L. Rea]

Okay, you asked....

HPTA Supraphysiological Overcompensation:

The Holy Grail of Optimized Natural Human Performance Enhancement



During the 70’s and early 80’s supplement makers had little to offer in the way of anything useful for athletes, okay, other than vitamins and poor quality protein powders that tasted like sweetened dog food. Well, actually it was mostly animal grade soy protein with sugar added so I guess it was.



In the 90’s, a few viable performance-enhancing options such as creatine monohydrate and whey protein made their way into the market thus finally offering health and performance oriented alike something of statistical value.

What Happened?
​

In today’s media-hysteria-managed environment, athletes, supplement companies and drug dealers alike are seen in the same shady light. Why? In the new millennium performance enhancement through supplementation became a science. (No joke, really!) As the better companies employed more real scientists, they became more apt at researching and marketing substances that truly could be said to be “steroid-like� in effect. And of course, the pharmaceutical industry, sports organizations and government agencies took interest. The pharma industry because of money, sports organizations because players wanted more, and the government because of both reasons.



It has to be a sad state of affairs when a society has reached a point in its ineptitude that government intervention is deemed necessary as a means of controlling individual choice for performance enhancement, or not, from over the counter supplementation. Yet the only qualification required for purchase of enough alcohol to kill ones self is 21 years of age and the capacity to say “Bud�.



After all, no one seems appalled by the unfair advantage performance enhancement drugs like Viagra™ (sildenafil citrate) and Cialis™ (tadalafil) allows cheaters. (Don’t get me started on the unfair advantages women with large breast augmentations have over post-nursing mothers…Okay, like I care)

We’re Not In Kansas Anymore…
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As a result of today’s media-hysteria-managed environment, everyone wants to write a tell-all book and government intervention, we have moved into an era of supplementation skepticism leaving only a few options left to truly innovative supplement makers. Well, at least those with an interest in the future of our industry and an authentic interest in the edge science can offer athletes (and every day normal people as well):



1) Work to maximize human performance through health promoting physiological optimization (WADA, IOC and pro-sports friendly)



2) Bring on greater government intervention and regulation for the entire sports and supplemental industry.



3) Move to Mexico where no one cares what you do to yourself…and take lots of Viagra or Cialis.

Where to Start
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The first and most important How-to answer in the optimization of human performance begins with HPTA Supraphysiological Overcompensation: The Holy Grail of optimized natural human performance enhancement.



Before I go on, realize that this is the catalyst for all of the good things you really want to happen if performance optimization is your goal…so take the time to read it!



The human body has the ability to naturally produce amazing amounts of anabolic goodies like testosterone, GH (growth hormone), IGF-1 (Insulin Growth Factor-1) and insulin. It also has the ability make more thyroid hormones and other fat burning substances than you could ever reasonably want (never met a reasonable bodybuilder but I did hear of one once)



In regard to everyone’s favorite naturally occurring man-making androgen, testosterone is king of the muscle building anabolics…and your body can make WAY more than you need through HPTA Supraphysiological Overcompensation.

Warning: Science Geek Stuff (That actually matters)
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Both men and women produce testosterone naturally, but here lets primarily focus upon the men. (I will show you a diagram of how the ladies do it as well anyway for the curious)



Endogenous (made inside the body) testosterone production is predominantly a result of, and governed by, the HPTA (Hypothalamus-Pituitary-Testes-Axis). It all begins with a gland located in your head called the hypothalamus when it releases a measured amount of GnRH (also known as LH-releasing hormone).



The small amount of GnRH then makes its way to the pituitary gland to tell it to kick out two other hormones called LH (Luteinizing Hormone) and FSH (Follicle-Stimulating Hormone). Nope, the job is not done yet.



Okay, LH and FSH then take a trip via the vascular system to the testes (testicles, “The Boy’s�, testes… whatever) and make contact with the Leydig cells and Sertoli cells …which results in testosterone synthesis and sperm production respectively.

HPTA Function Pathways
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The amount of GnRH, LH and FSH produced regulates the amount of testosterone, androstenediol and DHEA your body produces…or not. If the HPTA produces supraphysiological amounts of GnRH, LH and FSH, it actually also produces more performance enhancing goodies like testosterone, androstenediol and DHEA by way of overcompensation. Getting the idea here?



THAT is HPTA Supraphysiological Overcompensation.

The Question You Really Want To Ask…
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Why Don’t “My Boy’s� Do That Naturally?
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Like all things we really like in life, there is a series of checks and balances that keep things in control and limit the amounts of good stuff we can have (like girlfriends). In the case of HPTA-function and optimized testosterone production, it is due to 2 primary negative feed-back loops. (Most know this first one, but let’s recap to be sure).

Estrogen Negative Feed-Back Loop
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High estrogen levels are not the sole propriety of women with amazing sweater puppets and bizarre mood swings. Men produce it too, and in most cases, there is way too much in any man’s system than nature meant there to be. This also helps to explain way males produce less testosterone and sperm today than they did only 2 generations ago.



This is due significantly to un-natural (exogenous) exposure to the overabundance of plant-derived phytoestrogens (such as those found in soy products) and xenoestrogens in plastics and herbicides today.



Don’t get me started on chemically raised meats and pesticides, too.



Natural (endogenous) estrogen is predominantly made in the male body from the aromatization of endogenous (made inside the body) androgens (such as testosterone) into estrogens. This is the responsibility of an enzyme called aromatase that is present pretty much everywhere in the body…even the brain around the hypothalamus (remember that).



When too much estrogen interacts with the estrogen receptors of the hypothalamus, there is a negative feed-back loop that tells the gland that there must be too much testosterone as well. The result is a dramatic unhealthy reduction, or even shut-down, of the HPTA and girl status for the owner of the saggy-sack problem. But it gets worse…

Androgen Negative Feed-Back Loop
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The hypothalamus also has lots of androgen receptors for sensing the level of testosterone and other androgens circulating in the body. When too many androgen receptors of the hypothalamus become activated, there is a decrease or even total shut-down in GnRH release. This means that “The Boy’s� pretty much have nothing to do because the lack of GnRH release also means no LH or FSH release.



So the end result is your testes have no reason to produce testosterone or sperm…and no reason to optimize muscular activities, recovery or have sex. Hmmm, look bad, feel bad and not care. That is ugly.

Anabolic Steroid Users and Saggy-Sacks
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The reason most AAS users employ the drugs is to un-naturally increase their testosterone levels to 2-5 times what is so-called natural or normal. Of course the results are obvious: Increased muscle mass, decreased fat mass, a marked increase in metabolic rate, better focus, and improved performance in every manly area. The bad results are all of the negative side-effects from excessive estrogen and lipid issues that synthetic androgens can cause.



Normal total testosterone production for a healthy male is about 500-600ng/dl (too many are in the 200-350ng/dl range due to environmental estrogens alone), but some AAS users push the levels into the 2000-3000ng/dl plus area. As a result of all of this excess testosterone floating around the body, there is a lot of aromatization to estrogens and an overabundance of androgen receptors of the hypothalamus being over-stimulated. The outcome is obviously the loss of testicular function due to both negative feed-back loops occurring.



Many AAS users know that by decreasing the amount of circulatory estrogen, they are also able to somewhat decrease HPTA down-regulation. Post-cycle AAS therapy, in most cases, includes something to decrease estrogen levels and activity, and some other drug to replace LH. If done correctly the end result again is an increase in actual natural testosterone product 1-2 times above normal for a brief period.

Clomiphen, Anastrazole and HCG…Oh My
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(The Most common PCT)
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PCT stands for Post-Cycle-Therapy and refers to HPTA regeneration or stimulation. Anabolic steroid users and those looking to increase endogenous androgen production alike, have used this so-called stack almost like a religious rite not realizing there was an error in its structure.



Clomiphen Citrate is the generic name for Clomid ® which is a fertility drug used to stimulate ovulation in women and increase sperm production in men. Clomiphen citrate is actually a very weak estrogen in itself. It works by blocking more powerful and active estrogens from merging with the hypothalamic estrogen receptors. The end result is the hypothalamus “perceives� that there is less circulatory estrogen and responds by increasing GnRH release. In addition there is some degree of decrease in estrogen activity throughout the rest of the body as well for the same reason. As a rule 50mg daily for 2-3 weeks of clomiphen citrate has been noted as effective for this purpose.



Anastrolzole is a generic name for the drug Arimidex ®. This is an aromatase enzyme inhibitor that decreases conversion of susceptible androgens into estrogens. This action results in a decrease in total circulatory estrogen. As little as 1mg 3 times weekly post-cycle for 30 days has been shown to decrease estrogen by 50% and have some benefits in regard to HPTA regeneration due to its mopping up effect.



But this combination only helps clean up the effects of the Estrogen Negative Feed-Back Loop leaving the Androgen Negative Feed-Back Loop unaffected.



HCG refers to Human Chorionic Gonadotropin. This is a hormone that is produced by pregnant women and used in fertility medicine. In males, HCG has been shown to mimic LH thus administration results in direct stimulation of the testes resulting in minimal increases in sperm production and significant increases in testicular testosterone production. Interestingly enough, this pregnant woman’s hormone is effective to a point that some studies have shown it to be able to prevent testicular dysfunction during anabolic steroid use. But again, that is a whole other article. Most have realized notable HPTA recovery and/or androgen production stimulation form administering 1000iu HCG 3 times weekly for 21 days post-cycle.



Hmmm, still nothing to “positively� affect the Androgen Negative Feed-Back Loop.

Action/Reaction…And Things That Go Hump More In the Night
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The ideal situation would be the ability to decrease estrogen levels in the whole body while decreasing androgen activity of the hypothalamus specifically. Of course we would not want to decrease androgen receptor activity in other peripheral areas like muscle tissue, and we would want focused estrogen control around the hypothalamus to create the best performance enhancing synergy naturally. Can that be done? Of course it can, just as Nolvadex ® is way more specific to breast tissue, some really cool compounds are WAY more specific to the hypothalamus.



The result would be long term HPTA Supraphysiological Overcompensation and viable naturally occurring testosterone production at a significant and highly effective level. This would (and has) obviously allow for optimization of human male performance. That is a perfect example of correct application of the body’s natural health promoting Action/Reaction Factors.



If you have read this far, then you already realize that I have explained the physiological and environmental factors that foster an un-natural chain of events resulting in significant reduction and limitation for every male’s performance…in every aspect of the word.



If you are interested in legal and natural ways to optimize male physical and mental performance (and improve the fun of what goes Hump in the night) then read on.



We Had To Start Somewhere…

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Chrysin
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Sometime in the early 80’s Dan Duchaine proposed that a plant aromatase called Chrysin (Flavone X) was comparable in effect to the well-known biosynthesis inhibitor/anti-aromatase Cytadren (Aminoglutethimide). This was due to the structural similarities the two compounds possessed. Dan was sharp (he kept us all thinking), but he missed on this one. In truth Chrysin totally bombed out in the real-world as it is actually just another phytoestrogen making male users fat and less masculine.

AT
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Until recently the only well known and statistically effective OTC supplemental anti-aromatase for systemic (whole body) estrogen control was delta-4-10, 13-dimethyl-cyclopenta[a]phenantrene-3,6,17-trione (A.K.A. 4-androstene- 3,6,17-trione) or “AT� for short. (One trade name for it was Aromax™ by Applied Lifescience Research Industries Inc.).



One main concern with the “AT� structure is its potential conversion to the feminizing estrogens 6-keto-estrone and 6-keto-estradiol (Estradiol’s of any kind are as much as 10 times more powerful than estrogen’s). Naturally there is a dose dependant issue here which is a supplemental oxymoron: Low bioavailability means higher dosages needed, that in turn result in greater amounts of AT being converted to the feminizing estrogens 6-keto-estrone and 6-keto-estradiol. Read on, you will understand better…



Depending upon bodyweight and level of estrogens in a man’s body, at 600mg daily AT appears to be reasonably useful, and in truth it was the only viable option for sometime. The main limitation for this compound is that it has poor oral bioavailability (the reason for required dosages being above the half gram mark daily), and of course it only aids inhibition of the Estrogen-Negative-Feed-Back-Loop. This is not to say that it was not a useful compound. However, the Androgen-Negative-Feed-Back-Loop still remains the main limiting factor.

Synergy Is the Key to an Optimization Matrix
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There are some very effectual options currently coming to market that have viable research behind them that specifically address both the estrogen-negative-feed-back-loop and the androgen-negative-feed-back-loop on multiple levels.

3-O-WHO?
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6,17-dioxo-etiocholene-3-ol (A.K.A. 3-OHAT) is a natural occurring metabolite of the popular anti-aromatase supplement 4-androstene- 3,6,17-trione (AT) mentioned prior. It possesses a much longer half-life (stays active in the body longer) thus allowing for improved efficiency from a single daily dosage. Additionally it is noted as a non-androgenic aromatase inhibitor. This means that 3-OHAT is an excellent fast-acting long-term destroyer of the testosterone limiting Estrogen-Negative-Feed-Back-Loop…and does not stimulate androgen receptors of the hypothalamus and the Androgen-Negative-Feed-Back-Loop. Studies have shown that even acting alone, 3-OHAT increases HPTA activity resulting in more testosterone production via natural pathways in humans and animals.

ATD and Focus
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3,17-dioxo-etiochol-1,4,6-triene (A.K.A. ATD) has a prolonged affinity for the estrogen mediating aromatase enzyme. In fact, it is actually about 2.8 times more powerful than AT for this reason. So great, it is more powerful than AT and even more powerful than 3-OHAT in a different way. Big deal?



In vitro studies have shown ATD to be a powerful androgen receptor blocker of the hypothalamus…but not of peripheral androgen receptors. What’s this mean in English? It means that ATD blocks the Androgen-Negative-Feed-Back-Loop and aids in decreasing estrogen production while increasing natural testosterone production. (If you are paying attention and focusing a little here, I am sure the real point of this article just hit you)

Synergy
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There is a need for synergy in anything in life and physiological Action/Reaction Factors are no exception. As you know by stopping Both negative feed back loops, the hypothalamus will produce more GnRH which in turn means that the pituitary will produce more LH/FSH and “The Boy’s� will kick out a whole lot of male optimizing testosterone. Sounds good in theory?



Of course some studies have shown that the correct ratio of 3-OHAT and ATD administered to adult human males results in an average increase in bioavailable testosterone of up to 400% and a direct decrease in estrogens of an average 50%. (No joke!) Up to 4 times the man and half the girl is not a bad natural improvement for a lad.

Okay, But What About The Real World…
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I personally do not believe anything I cannot prove myself in the lab. As such we used 8 healthy males as human guinea pigs to test what the research claims to be factual. 4 acted as a placebo base-line group receiving 6 capsules daily of cornstarch, and the other 4 got the real deal consisting of a proprietary 50mg blend of both 3-OHAT and ATD. During the pre-administration period we tested for Total Testosterone, Free Testosterone and Estradiol, then tested again at 14 and 42 days.

Results:
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Placebo Group: No significant changes (Gee, are you surprised?) in total or free testosterone and estradiol.



Subject 1 (24 year old male)

Pre-testing:

Total Testosterone: 350ng/dl

Free Testosterone: 83.00pg/ml

Estradiol: 39pg/ml



14 Days

Total Testosterone: 1803ng/dl

Free Testosterone: 522.20pg/ml

Estradiol: 27pg/ml



42 Days

Total Testosterone: 2895ng/dl

Free Testosterone: 839.20pg/ml

Estradiol: <20

Subject 2 (33 year old male)

Pre-testing:

Total Testosterone: 538ng/dl

Free Testosterone: 129.0 pg/ml

Estradiol: 30pg/ml



14 Days

Total Testosterone: 988ng/dl

Free Testosterone: 233.0pg/ml

Estradiol: 22pg/ml



42 Days

Total Testosterone: 1416ng/dl

Free Testosterone: 421.3pg/ml

Estradiol: <20

Subject 3 (25 year old male)

Pre-testing:

Total Testosterone: 555ng/dl

Free Testosterone: 104.00pg/ml

Estradiol: <20



14 Days

Total Testosterone: 1624ng/dl

Free Testosterone: 405.7pg/ml

Estradiol: <20



42 Days

Total Testosterone: 1837ng/dl

Free Testosterone: 547.40pg/ml

Estradiol: <20

Subject 4 (51 year old male)

Pre-testing:

Total Testosterone: 584ng/dl

Free Testosterone: 13.40ng/dl

Estradiol: 47pg/ml



14 Days

Total Testosterone: 851ng/dl

Free Testosterone: 26.10ng/dl

Estradiol:



42 Days

Total Testosterone: 875ng/dl

Free Testosterone: 30.30ng/dl

Estradiol: <20




Test results showed a net increase in total and free testosterone ranging from 50-800% with a significant reduction in estradiol of about 50%. More importantly is that the elevation was maintained for a long enough period to allow notable benefits from a physiological stand-point (weeks, not just a few minutes). Huh, go figure, the studies are right.



Testosterone is the anabolic steroid that all other AAS (Anabolic-Androgenic-Steroid) are compared to…and your body can naturally and legally produce far more than you actually need. Most negative side effects come from the use of AAS, not from the excess of natural endogenous testosterone itself.



I would like to see the results from the same test subjects using the 50mg 3-OHAT/ATD proprietary blend with the addition of Agaricus bisporus extract (white button mushroom from a specific region) and 7b-hydroxy-DHEA. The Agaricus bisporus extract because the right method of extract provides some very effective site-specific aromatase enzyme inhibition, and the 7b-Hydroxy-DHEA because it is preferential physiological base compound for many good things. But we will save that for future articles.



Author L. Rea







References:

1) Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis. Kaplan ME, McGinnis MY. Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

2) 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.

3) J Steroid Biochem. 1986 Oct;25(4):593-600. Effect of 1,4,6-androstatriene-3,17-dione (ATD), 4-hydroxy-4-androstene-3,17-dione (4-OH-A) and 4-acetoxy-4-androstene-3,17-dione (4-Ac-A) on the 5 alpha-reduction of androgens in the rat prostate. Motta M, Zoppi S, Brodie AM, Martini L.

4) Horm Behav. 1989 Mar;23(1):10-26. Effects of ATD on male sexual behavior and androgen receptor binding: a reexamination of the aromatization hypothesis. Kaplan ME, McGinnis MY.
Department of Anatomy, Mount Sinai School of Medicine, CUNY, New York 10029.

5) Effect of steroid aromatase inhibitors on the catecholamine content of the hypothalamus of neonatally androgenized rats][Article in Russian] Nosenko ND, Reznikov AG.

6) J Steroid Biochem Mol Biol. 1992 Oct;43(4):281-7. In vitro potency and selectivity of the non-steroidal androgen aromatase inhibitor CGS 16949A compared to steroidal inhibitors in the brain.
Wozniak A, Holman SD, Hutchison JB. MRC Neuroendocrine Development and Behaviour Group, Institute of Animal Physiology and Genetics Research, Babraham, Cambridge, England.

7) J Clin Endocrinol Metab. 1993 Dec;77(6):1529-34. Differential effects of aromatase inhibition on luteinizing hormone secretion in intact and castrated male cynomolgus macaques. Resko JA, Connolly PB, Roselli CE, Abdelgadir SE, Choate JV. Department of Physiology, Oregon Health Sciences University, Portland 97201-3098.

8) J.Steroid Biochem. 1987 Sep;28(3):337-44 Studies on aromatase inhibition with 4-androstene-3.6.17-trione: Its 3-beta reduction and time dependant irreversible binding to aromatase with human placental microsomes. Numazawa M, Tsuji M, Mutsumi A. Tohoku College of Pharmacy, Sendai, Japan.

9) Biol Reprod. 1994 Dec;51(6):1273-8. Prenatal inhibition of aromatase activity affects luteinizing hormone feedback mechanisms and reproductive behaviors of adult guinea pigs. Choate JV, Resko JA. Department of Physiology, Oregon Health Sciences University, Portland 97201.

10) Biol Reprod. 2003 Feb;68(2):370-4. Estrogen synthesis in fetal sheep brain: effect of maternal treatment with an aromatase inhibitor. Roselli CE, Resko JA, Stormshak F. Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon 97201-3098, USA. [email protected]

J Nutr. 2001 Dec;131(12):3288-93.
White button mushroom phytochemicals inhibit aromatase activity and breast cancer cell proliferation.Grube BJ, Eng ET, Kao YC, Kwon A, Chen S. Division of Immunology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.

 

[milwood]

Thanks, "Lad"...

 

[Author L. Rea]

Yup.

 

[Alpha Dog]

Author, great article. :box:

Why do you think you are seeing such an increase in free testosterone? Most of the results I have seen from AI's do not show such a profound increase. Could it have something to do with the AR blockade from the ATD analog and the body producing less SHGB? Anotherwords, the blocking the negative feedback is preventing the bodies ability to metabolize the free test as quickly?