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posted by JohnnyB
JohnnyB posted this in response to a question on Intense-Training, I thought that it was a very well written of what hcg is used for by BB'ers.
ISN'T THAT THE TRUTH!!!
Most of it come from people that don't understand the reason for using HCG during the cycle. As we can see by the Bro that started this thread, not try to call you out or flame you Bro, it's a common mistake with lots of people that don't understand make, then you have people that add to the misconception and it really gets confusing. It is not used to stop you from shutting down or to stimulate test production, it is used to keep the boys alive, which in turn give you one less thing to recover from during PCT. I'm not the pro on this either, but I have researched it and used it as well.
Here's the problem with using 1500iu or more in one dose, it desensitizes the testes to LH, not a good thing when try to recover. All the protocols I've seen that are for post cycle HCG use, use doses of 1000iu or more, with the 1000iu being used ed. Which will pretty much guarantee you'll be in the same situation as a one time 1500iu dose, since HCG has an active life of 64 hours. The cause of the desensitization is from raised estrogen, grant it you could add nolva to the mix, but now you are in the place of adding drugs to combat a side effect. When this can be avoided by using smaller doses during the cycle, but if you are using it during PCT you'll already be on nolva or could add it for recovery, yes this is true, but I'll shade some light on that after the study. Here's the study where I got this info.
Posted by hhajdo at S’ology
Differential effect of single high dose and divided small dose administration of human chorionic gonadotropin on Leydig cell steroidogenic desensitization.
Smals AG, Pieters GF, Boers GH, Raemakers JM, Hermus AR, Benraad TJ, Kloppenborg PW.
This study compared the effect of a single high dose of hCG (1500 IU) with that of the same dose administered in multiple small doses (300 IU, once daily for 5 days) on Leydig cell steroidogenesis. Administration of a single high dose of hCG to seven healthy men raised the mean plasma testosterone (T) level to peak levels 2.1 +/- 0.2 (SEM) X the baseline value at 48 h. Thereafter plasma T decreased to below normal (0.7 +/- 0.1 X baseline) 7 days after the injection. The mean 17-hydroxyprogesterone (17-OHP) level peaked at 24 h (2.5 +/- 0.2 X baseline) and then also fell to a nadir value of 0.6 +/- 0.2 X baseline on day 7. Reflecting the early accumulation of 17-OHP over T, the 17 OHP/T ratio reached its maximum (1.6 +/- 0.1 X baseline) at 24 h at the same time when plasma estradiol [(E2) 4.4 +/- 0.6 X baseline] and the ratio E2/T (2.7 +/- 0.3 X baseline) achieved their maximal values. Administration of 1500 IU hCG in five divided doses of 300 IU daily increased the mean plasma T levels to peak value of 2.1 +/- 0.2 X baseline at 5 days and the levels remained elevated thereafter. The response of T as reflected by the area under the curve was almost twice as great as in the single dose study (2844 +/- 360 vs. 1647 +/- 214). In contrast to the single high dose experiment, mean plasma 17-OHP levels in the divided dose protocol did not peak at 24 h but only gradually increased. As the increase of T exceeded the 17-OHP increase at almost all time intervals, no accumulation of 17-OHP over T occurred as in the single dose experiment. Instead the 17-OHP/T ratio fell to a nadir value of 0.6 +/- 0.1 X baseline on day 7. The initial E2 peak was absent in the divided dose protocol and the E2/T ratio only marginally increased. Considering both experiments together a close relation was found between the hCG-induced increases in E2 and 17-OHP (r = +0.88, P less than 0.001), as well as the ratio 17 OHP/T (r = +0.64, P less than 0.02).
-----------------------------------
Think about this as well, HCG mimics LH, by using HCG during PCT you are mimicking LH to stimulate testosterone levels. This also sends a signal to the body that you have enough LH to stimulate testosterone production. So now you body thinks it's producing enough LH, so you're making the clomid and/or nolva of no effect to restoring your LH production. This is just my speculation, if someone has a study or some info that says different, go with it. I have come to this conclusion because of how the body signals itself on regulating the production of hormones.
We shut down our HTPA, because the body is telling itself that we have enough or more then enough testosterone, so it stops producing LH, then the testes athorpy, because of the negative feedback. So, yes your testosterone levels will be raised by the mimicked LH, but the clomid and/or nolva hasn't stimulated the raise of LH, because the body thinks it already has LH in the system to produce testosterone. So in theory, you could run PCT with HCG and never get you natural LH going to stimulate your natural testosterone levels, because your body told itself that it already had LH and didn't need to produce anymore. Basically what you have is the same as trying to get the HPTA going during a cycle with HCG, it's not going to happen. Body is signaling itself that there is enough testosterone already, no need to make more. Why would HCG mimicking LH be any different, when nolva and/or clomid are trying to stimulate LH, the body is telling itself it already has LH.
Here's a study showing nolva to work better then clomid, in stimulating LH.
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
---------------------
Do you guys see my point on how using HCG during PCT, isn't the best idea or using the 1000iu for 10 days before PCT, if you desensitizes the testes to LH, you're defeating the purpose of doing PCT. You need the testes to be sensitive to LH to get your natural testosterone back to normal. Trying to stimulate LH, when your are using a drug that mimics LH, doesn't sound like a good idea either.
We need to re-think PCT, the idea that 3-4 weeks is the standard of PCT and it works for all cycles, is not true, it may hold true for a beginner cycle of 400-500mg of test a week, but after that it's a hold new ball game. PCT should be run until your sex drive is back in full swing, this a good indicator that your natural test levels are back to normal.
I hope this didn't make it more confusing, this isn't the only way to use HCG, during a cycle in small doses to keep the boys alive, but it's the one I recommend and use, if that means anything
JohnnyB posted this in response to a question on Intense-Training, I thought that it was a very well written of what hcg is used for by BB'ers.
ISN'T THAT THE TRUTH!!!
Most of it come from people that don't understand the reason for using HCG during the cycle. As we can see by the Bro that started this thread, not try to call you out or flame you Bro, it's a common mistake with lots of people that don't understand make, then you have people that add to the misconception and it really gets confusing. It is not used to stop you from shutting down or to stimulate test production, it is used to keep the boys alive, which in turn give you one less thing to recover from during PCT. I'm not the pro on this either, but I have researched it and used it as well.
Here's the problem with using 1500iu or more in one dose, it desensitizes the testes to LH, not a good thing when try to recover. All the protocols I've seen that are for post cycle HCG use, use doses of 1000iu or more, with the 1000iu being used ed. Which will pretty much guarantee you'll be in the same situation as a one time 1500iu dose, since HCG has an active life of 64 hours. The cause of the desensitization is from raised estrogen, grant it you could add nolva to the mix, but now you are in the place of adding drugs to combat a side effect. When this can be avoided by using smaller doses during the cycle, but if you are using it during PCT you'll already be on nolva or could add it for recovery, yes this is true, but I'll shade some light on that after the study. Here's the study where I got this info.
Posted by hhajdo at S’ology
Differential effect of single high dose and divided small dose administration of human chorionic gonadotropin on Leydig cell steroidogenic desensitization.
Smals AG, Pieters GF, Boers GH, Raemakers JM, Hermus AR, Benraad TJ, Kloppenborg PW.
This study compared the effect of a single high dose of hCG (1500 IU) with that of the same dose administered in multiple small doses (300 IU, once daily for 5 days) on Leydig cell steroidogenesis. Administration of a single high dose of hCG to seven healthy men raised the mean plasma testosterone (T) level to peak levels 2.1 +/- 0.2 (SEM) X the baseline value at 48 h. Thereafter plasma T decreased to below normal (0.7 +/- 0.1 X baseline) 7 days after the injection. The mean 17-hydroxyprogesterone (17-OHP) level peaked at 24 h (2.5 +/- 0.2 X baseline) and then also fell to a nadir value of 0.6 +/- 0.2 X baseline on day 7. Reflecting the early accumulation of 17-OHP over T, the 17 OHP/T ratio reached its maximum (1.6 +/- 0.1 X baseline) at 24 h at the same time when plasma estradiol [(E2) 4.4 +/- 0.6 X baseline] and the ratio E2/T (2.7 +/- 0.3 X baseline) achieved their maximal values. Administration of 1500 IU hCG in five divided doses of 300 IU daily increased the mean plasma T levels to peak value of 2.1 +/- 0.2 X baseline at 5 days and the levels remained elevated thereafter. The response of T as reflected by the area under the curve was almost twice as great as in the single dose study (2844 +/- 360 vs. 1647 +/- 214). In contrast to the single high dose experiment, mean plasma 17-OHP levels in the divided dose protocol did not peak at 24 h but only gradually increased. As the increase of T exceeded the 17-OHP increase at almost all time intervals, no accumulation of 17-OHP over T occurred as in the single dose experiment. Instead the 17-OHP/T ratio fell to a nadir value of 0.6 +/- 0.1 X baseline on day 7. The initial E2 peak was absent in the divided dose protocol and the E2/T ratio only marginally increased. Considering both experiments together a close relation was found between the hCG-induced increases in E2 and 17-OHP (r = +0.88, P less than 0.001), as well as the ratio 17 OHP/T (r = +0.64, P less than 0.02).
-----------------------------------
Think about this as well, HCG mimics LH, by using HCG during PCT you are mimicking LH to stimulate testosterone levels. This also sends a signal to the body that you have enough LH to stimulate testosterone production. So now you body thinks it's producing enough LH, so you're making the clomid and/or nolva of no effect to restoring your LH production. This is just my speculation, if someone has a study or some info that says different, go with it. I have come to this conclusion because of how the body signals itself on regulating the production of hormones.
We shut down our HTPA, because the body is telling itself that we have enough or more then enough testosterone, so it stops producing LH, then the testes athorpy, because of the negative feedback. So, yes your testosterone levels will be raised by the mimicked LH, but the clomid and/or nolva hasn't stimulated the raise of LH, because the body thinks it already has LH in the system to produce testosterone. So in theory, you could run PCT with HCG and never get you natural LH going to stimulate your natural testosterone levels, because your body told itself that it already had LH and didn't need to produce anymore. Basically what you have is the same as trying to get the HPTA going during a cycle with HCG, it's not going to happen. Body is signaling itself that there is enough testosterone already, no need to make more. Why would HCG mimicking LH be any different, when nolva and/or clomid are trying to stimulate LH, the body is telling itself it already has LH.
Here's a study showing nolva to work better then clomid, in stimulating LH.
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.
Vermeulen A, Comhaire F.
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
---------------------
Do you guys see my point on how using HCG during PCT, isn't the best idea or using the 1000iu for 10 days before PCT, if you desensitizes the testes to LH, you're defeating the purpose of doing PCT. You need the testes to be sensitive to LH to get your natural testosterone back to normal. Trying to stimulate LH, when your are using a drug that mimics LH, doesn't sound like a good idea either.
We need to re-think PCT, the idea that 3-4 weeks is the standard of PCT and it works for all cycles, is not true, it may hold true for a beginner cycle of 400-500mg of test a week, but after that it's a hold new ball game. PCT should be run until your sex drive is back in full swing, this a good indicator that your natural test levels are back to normal.
I hope this didn't make it more confusing, this isn't the only way to use HCG, during a cycle in small doses to keep the boys alive, but it's the one I recommend and use, if that means anything
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