hcg and suppression
- 06-19-2004, 02:11 AM
- 06-19-2004, 02:25 AM
- 06-19-2004, 04:48 AM
I don't think that anything will prevent suppression except abstinance from using gear. Ancilliaries are only used to help with recovery as Matt has stated.
06-19-2004, 12:13 PM
I think the best way to explain it is that supplemental test (AS, PH) will cause shutdown via hpta disruption. In lay terms, one's gonads become inactive over the course of the cycle.
HCG itself does cause suppression, but it mimics LH, which keeps the gonads "primed" and functioning during a cycle....... I.E. they won't shrink from disuse.
Part of the problem over a long cycle is bringing the gonads back to full size and production. While Clomid and Nolva cause the hpta to begin the process of recovery, generall speaking, the longer the gonads have been in a state of disuse, and the more they've atrophied, the longer it takes to fully recover. I've known guys who have been on AS for so long (25 years ago, long before the days of hcg, clomid and nolva) they literally could not find their gonads they atrophied so badly.
I personally feel a lot better while taking hcg. While Nolva works well for me, it's that period of 1-2 weeks of waiting for it to restart production that I feel like crap. In my case, HCG goes a long way toward helping me retain more from a cycle. But some guys don't like it for one reason or another. Like everything else in life, your mileage will vary.
06-19-2004, 12:40 PM
HCG won't suppress by itself. It has 2 feedback loops (short and long) but it seems one doens't exert its effects in humans (as it did in animals). It was once thought that since it does mimic LH and your supplying the body with an exogneous hormone that suppression will occur but in recent studies they clarify the difference between previous studies.
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.
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.
It seems that the trouble with HCG is when your suppressed but the use of androgerns has discontinued (initial PCT). This might cause a prolonged suppression initially but the long term results are probably better response from the testes to increased LH. Bottom line? Use during your cycle.
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