ATD instead of HCG?
- 08-10-2005, 08:53 AM
- 08-10-2005, 08:53 AM
c'mon down, Author! When you get a chance, we'd all like some help on this one. And if anyone on the ALRI team cando so, help us out! Thanks!
08-10-2005, 08:56 AM
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08-10-2005, 09:03 AM
- On testicular size and HPTA function - I have repeatedly said that nut size is not THE indicator of HPTA function. The best way to describe this is looking at HCG. It increases testicular size, but actually is SUPPRESSIVE of HPTA function while it and its metabolites are active.
- On suppression/shutdown - Is anyone else sick and tired of people using hormones but whining about HPTA suppression?
08-10-2005, 09:12 AM
HCG isn't really that suppressive. The initial thought was based on animal studies but that effect wasn't seen in humans.
Inability to demonstrate an ultrashort loop feedback mechanism for luteinizing hormone in humans.
Kyle CV, Griffin J, Jarrett A, Odell WD.
Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.
hCG has biological properties similar to those of LH, but can be measured separately from LH by current radioimmunometric assays. To investigate the possible existence of an autoregulatory mechanism for LH in humans, we compared the basal LH concentrations and the LH response to a GnRH stimulus with and without prior administration of hCG. On two separate occasions, at least 1 week apart, six normal (eugonadal) males and six normal postmenopausal females were given, in random order, either 10,000 IU hCG or saline followed by iv injection of a 200-micrograms bolus of GnRH. Blood samples were then taken 30, 60, 90, 120, 180, 240, and 300 min after GnRH. Serum concentrations of LH and hCG were measured at each time by two monoclonal antibody sandwich assays developed in our laboratory. After exogenous hCG, serum hCG concentrations rose rapidly to 200-500 IU/L (15,000-35,000 pg/mL) in both the men and women, remaining at this high level throughout the study. In the men, sex steroid concentrations did not change in response to the hCG during the 9 study hours. Compared to saline-treated controls, hCG had no significant effect in either men or postmenopausal women on the basal LH concentration or the response to a GnRH bolus, as determined by peak response and area under the LH/time curve between 0-300 min after GnRH. We conclude that an ultrashort loop feedback mechanism for LH on its own secretion does not exist in humans, as assessed by the present protocol.
Endogenous luteinizing hormone surges following administration of human chorionic gonadotropin: further evidence for lack of loop feedback in humans.
Nader S, Berkowitz AS.
Department of Obstetrics, Gynecology and Reproductive Sciences, University of Texas Medical School, Houston 77030.
The existence of inhibitory short- and ultrashort-loop feedback mechanisms for luteinizing hormone (LH), while documented in animals, has been questioned in humans. Since human chorionic gonadotropin (hCG) binds to LH receptors but can be distinguished from LH in immunoassays, it is possible to identify LH surges in the face of exogenously administered hCG. The present study demonstrates LH surges at midcycle in normal volunteers and in women undergoing controlled ovarian hyperstimulation, given hCG. This provides further evidence for lack of loop feedback control of LH secretion in humans.
Testicular size is more dependent on Sertoli cells (as in production of sperm) as opposed to Leydig cells. You could have normal production of testosterone and still have "shrinkage". Only way to know is bloodtest.
For answers to board issues, read the Suggestion and News forum at the bottom of the main page.
08-10-2005, 09:20 AM
Sweet. Thanks Bobo.
I also would like to point out that the ol boys just drop in outta nowhere mid-cycle sometimes.
I just hate to see people think that feeling their balls is a substitute for bloodwork.
08-10-2005, 10:59 AM
Originally Posted by ryansm
I don't think I could have put that in beelzelanguage any better. Maybe a beer analogy
08-10-2005, 12:48 PM
I guess my bottom line is that I'm using some UH that I have during a long cycle, instead of some HCG that I have. I really want to know if this is a good or bad idea. I trust Author's suggestion, but of course at this point, there is still a lot of speculation, not a lot of concrete proof. Anyone think I should go conservative and switch to HCG? I'm not far along enough to have an issue either way, so I have some time to decide really. I do believe that the ATD is absolutely working well for estrogen control and the boys are fine to this point. I'm just thinking maybe I'll use HCG towards the end.Thoughts?
08-10-2005, 01:20 PM
the thing is, ATD may be as good as HCG for restoring your HPTA function following the cycle - but i doubt it would be as good as mimicking swale's protocol of 250ius of HCG x 2 times a week.
just my opinion, obviously no evidence suggests either way.
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08-10-2005, 01:40 PM
Originally Posted by CEDeoudes59
Agreed. We just don't have enough supporting data to make a call either way with much conviction. My hope is that people will continue to use ATD during their cycles and post bloodwork immediately following so that we gather the necessary data. Until that point, the safest protocol would be to stick to HCG during a cycle (if you literally don’t feel like putting your nuts on the line and being one of the gunieapigs). If you want to be extremely conservative, I see no reason to not run both during a cycle. At the least, ATD will keep estrogen in check.
08-13-2005, 11:27 AM
Bow, I read that article ALR has on readthecore and it does say that its affinity to binding to the hypothalamus is higher than in other tissues. This may very well be the case, but does anybody have a study showing this? The below articles are very informative but dont explicitly state this, unless Im just reading it wrong.Originally Posted by bow
08-13-2005, 12:12 PM
I'm just gonna say again that I willl patiently await ALR's further explanation. I know he is busy, but I expect at some time he'll let us know a bit more, since he opened this idea up publicly. However, I'll say in honesty that I wish the ALRI team would be a bit more vocal on the subject. Or perhaps they simply don't know yet either. I've asked repeatedly for info, at least particulars on the ALRI products (HOT/HOTter), yet don't get responses, unfortunately...
08-13-2005, 12:21 PM
Not too surprising, from what I've seen, he doesn't explain much of anything, nor use references that actually hold any value.
08-13-2005, 12:53 PM
No, but ALRI stuff works. Like him or not (I personally like the guy), his stuff WORKS.
So I use his stuff.
08-13-2005, 03:03 PM
Most of it works, prostan has not been all the rage it was cracked up to be unless stacked with something stronger, but no supplement line is perfect. Just like many other supplement companies who are releasing designer supplements, they are just reinventing the wheel. DMT has been around since the 70's.Originally Posted by N4cer
*Not trying to be a smart ass, just stating an observation*
08-13-2005, 03:04 PM
And just so you understand, I have a bottle of E-Max at my house, so I use his stuff too.Originally Posted by N4cer
08-13-2005, 04:25 PM
actually I have always found Author to be quite willing to discuss questions and explain things in the past. Same with the ALRI team. This ATD issue, however seems to be an exception. I've been posting queries about ALR's take on ATD and the HCG issue (stemming from the "Core" article), as well as questions on dosing requirements and ATD content of UH/ HOTter for over 2 weeks in a number of threads (and even in PM's). Apparently either nobody knows or nobody's telling!Originally Posted by Onslaught
08-13-2005, 05:08 PM
My experience with Author and the ALRI team is that they do not comment on the board on a daily basis. Usually they are not heard from for a number of days and then appear to answer as many of the questions as they can. When they do answer I have found them to be helpful and friendly. I think we were coming to the end of one of their "few day" absent periods when this issue about the reporter contacting them started and since they have not been heard of except in regard to that issue. I imagine that some things will change this week when their new site goes up.
Originally Posted by milwood
08-13-2005, 05:50 PM
You pretty much hit the nail on the head. You guys just need ti chill til that thing blows over.Originally Posted by Mr.50
08-14-2005, 01:19 AM
08-14-2005, 12:21 PM
Originally Posted by Sky9
There is a study to support the notion that atd demonstrates tissue preference, at least in terms of aramotase activity. I posted this a while back in this thread:
ATD and site-specific androgen receptor agonists
J Clin Endocrinol Metab. 1984 Dec;59(6):1088-96.
Inhibition of aromatization stimulates luteinizing hormone and testosterone secretion in adult male rhesus monkeys.
Ellinwood WE, Hess DL, Roselli CE, Spies HG, Resko JA.
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.
08-14-2005, 12:35 PM
Another interesting development came to light recently at Avant. The study below was recently posted in this thread:
This may explain why some are seeing increased test levels while administering exogenous hormones and experiencing a decrease in LH and FSH. Could ATD be giving a false result for an increase in test? Perhaps this explains Anarchy’s bloodwork and ATD in no way directly stimulates the testies. Its worth discussion.
Steroids. 1980 Dec;36(6):717-21.
Immunological interference of the synthetic aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) and its metabolite(s) in the radioimmunoassay for testosterone.
Donaldson MD, Forest MG.
Radioimmunoassay (RIA) for testosterone (T) in unchromatographed plasma extracts from ATD-treated rats gave spuriously high values for T. Cross-reaction and chromatographic studies subsequently showed that ATD and, to a much greater extent, its metabolite(s) were responsible for this overestimation. Celite column chromatography proved to be an effective way of separating T from ATD and its product(s) of metabolism.
08-14-2005, 01:05 PM
bow, you highlighted the least interesting part of the last study you posted, as far as this discuss goes, the following is of way more interest to us:
Granted, these are rat studies and done in vitro, take this together with another study showing anti-androgenic activity in the brain and we have ourselves a SARM.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.
08-14-2005, 03:47 PM
Originally Posted by Onslaught
I highlighted the part of the study that addresses the question asked (with regards to preferential tissue sensitivity).
There is no question (as emphasized by the section of the study you posted) that we are far from proving ATD is a hypothalamic site specific ar agonist. My argument with the thread I linked above is exactly that the studies are contradictory and far from being conclusive.
08-14-2005, 03:49 PM
But the problem here is that it appears there is at least the possibility that ATD is not really raising Test at all but just giving a false positive???? That is how I read it but maybe I am missing something. I can say though that the boys really felt much fuller to me when I was on Ultra Hot. I know tha is subjective but it was quite noticable.
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