Ghosting
Guest
So I garthered from Uncle Bruces post and the ALRI site that estrogen is still around during the cycle and its the neg feedback for the hypothalamus. Couldnt you take UHer on cycle to boost T up for gains and get a head start on PCT?
Alpha Dog
Obese Member
Ghosting said:
Androgens act largely negatively at the AR at the hypothalamus to limit GnRH. Estrogen influences the HPTA feedback loop primarily at the pituitary by influencing its sensitivity to GnRH to produce LH and FSH. So, keeping estrogen to a minimum during a cycle will keep the pituitary responding, but if the hypothalamous is shut down due to overstimuli of exogenous androgens, it is a moot point.
Ghosting
Guest
Oh the hypoothalamus shuts down? I didnt know that.bow said:
Alpha Dog
Obese Member
Ghosting said:
Hence the beauty of the concept of a site specific ar agonist. If it turns out that ATD is effective in this regards, then Ultra Hotter would help prevent shutdown from preventing inhibition at both the hypothalamous (androgen sensitive) and the pituitary (estrogen sensitive).
UGLY
New member
Please correct me if I am wrong, but I thought ultra hot and hotter were supposed to circumvent both the estrogen and the androgen negative feedback loops. According to the write-up on Invalid Link Removed, atd is supposed to be a "site-specific (like the hypothalamus) androgen receptor agonist." Meaning that the hypothalamous doesn't detect the excess androgens.bow said:
200wannabe
Board Supporter
Im still waiting to hear experiences of people who have run it on cycle for that purpose. Do you know of any logs Bow?
milwood
Registered User
anyone hip to the idea which has suggested that HOT/HOTTER (when used on cycle) can actually be used instead of HCG? If so, is it specifically because of the ATD content, and if that is so, what amount of ATD is suggested for this purpose? I know you kinda touched on this, Bow, but I wonder if there are any others who feel this is the case. Thanks.
milwood
Registered User
yeah, since ALRI's HOT is a proprietary blend, I can't get a read on how much ATD is in a serving, and therefore how much is suggested (ATD-wise) for a fair HCG swap. Maybe someone from the ALRI team could help here. For example, if I want to use ATD instead of HCG in a cycle, how many mgs of ATD do I want per day? And how much ATD is in a 3-cap suggested serving of HOT or HOTTER (or in a 4-cap suggested dose on that chart in the CORE article)? Thanks for anyone in the know.natiels said:
Anarchy939
Member
From experience, Ultra HOT (the original) kept my testosterone and free testosterone levels up, my estradiol (the bad estrogen) down, but my LH and FSH both bottomed out. So my theory is that somehow HOT mimics LH's mode of function by stimulating the production of testosterone without the necessity of natural LH, much like HCG. I believe this keeps the boys sensitive to LH, so when androgens are discontinued, they can readily accept the LH and produce testosterone.
While I believe that Ultra HOT (and HOTter for that matter) block the androgen negative feedback loop to some degree, they aren't powerful enough to fully eliminate the suppression of LH and FSH while on cycle. It does however block enough of the feedback loop for your LH and FSH to recover post-cycle while keeping free and total test up and estrogen down Post-Cycle.
Just my experience and theory...
While I believe that Ultra HOT (and HOTter for that matter) block the androgen negative feedback loop to some degree, they aren't powerful enough to fully eliminate the suppression of LH and FSH while on cycle. It does however block enough of the feedback loop for your LH and FSH to recover post-cycle while keeping free and total test up and estrogen down Post-Cycle.
Just my experience and theory...
Anarchy939
Member
Not sure about ATD dosing particularly, as I am not 100% on the dosage of ATD in the original formula per-cap. I took 4 caps per night while on and stayed with 4 for the first 2 weeks of PCT. Just last night I started using the new formula HOTTER at 3 caps each night to continue with my PCT. I think I heard somewhere that HOT has like 12.5mg/ATD per cap or so, so maybe 50mg ATD? I am a little unsure as to the exact amount.. I feel that the dose of ATD is more than likely variable with each individual and his/her sensitivity to androgens and level of shutdown reached with various compounds. For example, something like Max LMG wouldn't warrant as hefty of a dose of ATD as something heavily suppressive like M1T or 1-T. I may be wrong alltogether, but I am just trying to piece together what makes sense based on my experience running ATD from Ultra HOT.milwood said:
Ghosting
Guest
Im a bit of a noob to endocrinology talk, so bear with me. Are you guys saying you can use ATD in place of HCG? Other than ALR's methylated ATD, I thought it had poor b.v. (3%). I wasnt aware there was a stand alone brand or that you could even run it without 3-OHAT.?.?
Alpha Dog
Obese Member
Based on my current cycle, I would guess 50 mg’s day to be somewhere in the correct neighborhood.
I am on a six week cycle of tren/test-prop with prostanazol for the first three weeks and sd for the second three weeks. I have been supplementing with ATD throughout the cycle (25 mg’s 12 hours apart). Today is exactly the four week mark. So far, libido is still strong and I have experienced no noticeable testicular atrophy.
I am actually quite surprised at the results. Yes, blood work would go a long way to confirming my suspicions, but I suspect ATD is very useful at preventing/delaying testicular shutdown. I have a considerable amount of experience running four week cycles (this is my first six weaker) and I am familiar with the degree of testicular atrophy associated with a test/tren combo. What’s even more interesting is that with Tren along with ATD, I should be experiencing hpta shutdown simply due to over stimulation of the progesterone receptor. But again, I have experienced not noticeable atrophy or loss of libido.
Please also note that I was one of the first skeptics when it was claimed that atd was potentially a site specific ar agonist. I decided to run it during this cycle to test the theory for myself.
Invalid Link Removed
I am on a six week cycle of tren/test-prop with prostanazol for the first three weeks and sd for the second three weeks. I have been supplementing with ATD throughout the cycle (25 mg’s 12 hours apart). Today is exactly the four week mark. So far, libido is still strong and I have experienced no noticeable testicular atrophy.
I am actually quite surprised at the results. Yes, blood work would go a long way to confirming my suspicions, but I suspect ATD is very useful at preventing/delaying testicular shutdown. I have a considerable amount of experience running four week cycles (this is my first six weaker) and I am familiar with the degree of testicular atrophy associated with a test/tren combo. What’s even more interesting is that with Tren along with ATD, I should be experiencing hpta shutdown simply due to over stimulation of the progesterone receptor. But again, I have experienced not noticeable atrophy or loss of libido.
Please also note that I was one of the first skeptics when it was claimed that atd was potentially a site specific ar agonist. I decided to run it during this cycle to test the theory for myself.
Invalid Link Removed
Anarchy939
Member
Yeah, Running HOT with 3/4 of my last cycle sure has made pct a kick-back. I have continued to get stronger, while simultaneously losing the bloat/fat/water I gained while on. I am still up about 7lbs, all of which is solid at this point. My body fat is lower than it was pre-cycle at this point, and my waist is about 1/2" smaller than pre-cycle. ATD kicks ass! Hell, if it makes all my PCT's run this nicely, I don't care if I have to fork out a lot of cash just to get enough to run while on and for PCT.. IMHO its sure worth the extra penny to not have the PCT blues...ryansm said:
200wannabe
Board Supporter
bow said:
Bow, are you planning on running bloodwork?
Alpha Dog
Obese Member
Syr said:
Depends. If ATD is truly a site specific ar agonsit, limiting supplmentation to the last two weeks of a cycle is going to be far less beneficial than supplmenting throughout the cycle. Simply, if you are already shut down (or inhibited to some larger degree), I highly doubt ATD is going to stimulate LH production in the presence of any highly adrogenic exogenous hormones.
If on the other hand ATD is mimicking LH and is somehow directly stimulating the leydig cells (as suggested by Anarchy), then supplementing with ATD during the last two weeks of any cycle is going to accelerate recovery post cycle.
Unfortunately, we just don't know until we see more blood test results. Thus, if you want to play it safe, supplement throughout the cycle. At worst, if both theory's fail to pan out, ATD will help to keep estrogen in check during a cycle.
