would you recommend hcg with this cycle

[hollaatyoboy]

6 ft 215 12% bf this will be my third cycle

1-15 test e 750 ew
1-13 deca 400 ew
1-5 dbol 40 ed
17-20 clomid pct




i was wondering if i should throw in some hcg or will the clomid pct be adequate

[hosam4ever]

for 15 week cycle hcg is amust during the cycle & b4 pct

[hollaatyoboy]

how often and how many ius

[hosam4ever]

its ur duty 2 do the search ull find tons of info just type hcg in the search panel & enjoy ur time

[hollaatyoboy]

i was thinking 300-500 ius a week 1-16

[hollaatyoboy]

or should i carry the hcg all the way through pct

[Unoid]

I'm doing a similar cycle.
I'll do HCG twice.

week 6 and 12.
taking 3 shots those weeks of a split up 5000iu amp.

Or if you're able the week 1-15 is ideal.

[Mista Massive]

the main thing with HCG is watch and see how u go. if you begin to notice atrophy then begin using if not, i don't see why u should waste it. everyone is different. but more likely than not with such a cycle consisting of more than 12 weeks, you will probably need it

[FlyByU]

the main thing with HCG is watch and see how u go. if you begin to notice atrophy then begin using if not, i don't see why u should waste it. everyone is different. but more likely than not with such a cycle consisting of more than 12 weeks, you will probably need it

The problem with that is that it's very hard to judge testicular atrophy. The pituitary reduces its release and then totally stops its release of LH as a result of exogenous testosterone administration. This means that less testosterone is released by the leydig cells. HCG is a LH analogue. It gives a much more sustained release of LH than the pituitary produces naturally. Studies have shown that to avoid testicular atrophy, a minimum of 1050iu of HCG per week must be taken. This works out to 300iu HCG eod. Ideally, that is the dose everyone should be taking from day one until the end of the cycle, regardless of the cycle length. Remember that LH gets suppressed very soon after exogenous hormone administration.

[hugovsilva]

When I go over 10 weeks I usually run it mid cycle and during pct. Mid cycle 10 days at 500iu/day and pct 20days 500iu/day. And like this I use all the 3 5000iu amps.

[FlyByU]

HCG shouldn't be run during PCT because it is very suppressive. During PCT you want your natural LH to kick back in. That won't happen if u take HCG.

[hosam4ever]

when we say during pct we mean the period befor clomid therapy

[hugovsilva]

HCG shouldn't be run during PCT because it is very suppressive. During PCT you want your natural LH to kick back in. That won't happen if u take HCG.

Better read this.

Tnis was taken off A. Roberts PCT, which I have used and found to be the best pct i tried so far.

"HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman’s hormones (can anything really be said to control a pregnant woman’s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it’s not all that simple.

Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won’t be very effective. Unfortunately, this lack of an increase in testosterone doesn’t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it’s important to me and I suspect most men as well.
It would also appear that HCG works very well when it’s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)

This suggests that a pre-exposure to normal LH levels or gonadatropins in general is necessary for HCG-induced Leydig Cell desensitization. This, of course is not a problem for us, as we’ll be using it when LH/Gonadatropin levels are very low anyway …we just need to stop using it before we regain normal function, or it will work against us eventually. (19) (20). Luckily, the temporary Anabolic steroid induced hypogonadism that is experienced after a cycle basically allows us to respond to HCG like anyone with low LH levels (21), and thus, as I told you, a lot of the possible inhibitory effect of HCG is not going to be relevant because there was no prior “priming” by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during PCT, when we need to get back some HPTA function, and not when we have levels of gonadatropins high enough to cause HCG-induced desensitization.

But are we still risking some inhibition and possibly delaying our recovery by using HCG? Probably not…you see, some studies in humans have shown that HCG does not actually have a direct effect on inhibiting LH release in men (22)(23), but rather (probably) works to inhibit LH secretion indirectly, simply by stimulating the production of testosterone (thus activating the negative feedback loop). Another factor involved is the induction of testicular aromatase, which raises estrogen levels, again causing inhibition. Unfortunately, yet another process, the downregulation of the Leydig Cell LH receptor itself, seems to also play a role in high dose HCG testicular desensitization. This is also done by HCG actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) to testosterone (24). Nolvadex actually stops this blocking-action of HCG from taking place (25). Most likely, because of Nolvadex’s direct antiestrogenic effect and LH-upregulating effect on the Pituitary, suppression of gonadotropins via HCG is (25) almost totally stopped with concurrent administration of Nolvadex! So if we Use Nolvadex and we are only using HCG when we are low in gonadatropins, we won’t be inhibited by it at all! Right?

Well…maybe…but there’s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well…we can use low doses (300iu or so) to avoid some of that major spike in estrogen, and thus cause far less inhibition from the HCG (26). Of course, I’d want to use a bit more HCG per injection (500iu), if I could, to get my body functioning fully more quickly, and lose less of my gains. Maybe we can get away with taking some Vitamin E with our HCG, since it increases the responsiveness of plasma testosterone levels to HCG, making them significantly higher during vitamin E administration than without it (27). So we can get a better
response with our HCG by taking Vitamin E (I recommend 1,000iu/day), but that doesn’t get rid of the problem that we have, which is the estrogen increase the HCG will cause.

Lets solve that pesky estrogen problem now….

Lets add in an Aromatase Inhibitor! Which one, though? Well, since we are already using Nolvadex, we can’t use Letrozole or Arimidex, as the Nolvadex will actually greatly decrease the blood plasma levels of them (28)!

So we have to use Aromasin (exemestane) as our AI, because it’s an aromatase inactivator, meaning it makes estrogen receptors useless, and instead of just inhibiting production (as an anti-aromatase would do) it cuts off production totally. Aromasin can also cause androgenic sides (29)(30)(31), which may help to elevate your mood while you are on PCT. This final drug in my recommended PCT can effectively remove up to about 85%+ of estrogen from your body (32). Most importantly, using Aromasin together with Nolvadex doesn’t reduce exemestane’s effectiveness (33). So now, I think the problem of ANY inhibition possible with HCG is solved, and we can use that 500iu/day dose that I wanted to use previously.

With this PCT, there will be a rapid increase in LH, FSH, and testosterone, as well as almost a complete block on all the factors that could be causing your natural hormones to be delayed in returning to baseline. For this reason, I feel that the second your cycle is over is when you should start this PCT (a week after your last shot, or the day after your last pill is fine). Remember, waiting for some of the extra androgens you’ve been taking to leave your body is nonsensical, as we want to start recovery as soon as possible to retain maximum gains. There is no evidence to suggest waiting any length of time after your cycle is over will increase PCT effectiveness…it simply prolongs the time you aren’t doing anything positive to regain your natural hormones. And how long do we run this for? Well…we need to stop the HCG relatively soon for reasons discussed earlier. But the Nolvadex, and Aromasin can be used for awhile longer..."

[FlyByU]

Better read this.

Tnis was taken off A. Roberts PCT, which I have used and found to be the best pct i tried so far.

"HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman’s hormones (can anything really be said to control a pregnant woman’s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it’s not all that simple.

Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won’t be very effective. Unfortunately, this lack of an increase in testosterone doesn’t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it’s important to me and I suspect most men as well.
It would also appear that HCG works very well when it’s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)

This suggests that a pre-exposure to normal LH levels or gonadatropins in general is necessary for HCG-induced Leydig Cell desensitization. This, of course is not a problem for us, as we’ll be using it when LH/Gonadatropin levels are very low anyway …we just need to stop using it before we regain normal function, or it will work against us eventually. (19) (20). Luckily, the temporary Anabolic steroid induced hypogonadism that is experienced after a cycle basically allows us to respond to HCG like anyone with low LH levels (21), and thus, as I told you, a lot of the possible inhibitory effect of HCG is not going to be relevant because there was no prior “priming” by circulating gonadotrophins. This is great news for us, because we are going to be using HCG during PCT, when we need to get back some HPTA function, and not when we have levels of gonadatropins high enough to cause HCG-induced desensitization.

But are we still risking some inhibition and possibly delaying our recovery by using HCG? Probably not…you see, some studies in humans have shown that HCG does not actually have a direct effect on inhibiting LH release in men (22)(23), but rather (probably) works to inhibit LH secretion indirectly, simply by stimulating the production of testosterone (thus activating the negative feedback loop). Another factor involved is the induction of testicular aromatase, which raises estrogen levels, again causing inhibition. Unfortunately, yet another process, the downregulation of the Leydig Cell LH receptor itself, seems to also play a role in high dose HCG testicular desensitization. This is also done by HCG actually blocking the conversion of 17 alpha-hydroxyprogesterone (17 OHP) to testosterone (24). Nolvadex actually stops this blocking-action of HCG from taking place (25). Most likely, because of Nolvadex’s direct antiestrogenic effect and LH-upregulating effect on the Pituitary, suppression of gonadotropins via HCG is (25) almost totally stopped with concurrent administration of Nolvadex! So if we Use Nolvadex and we are only using HCG when we are low in gonadatropins, we won’t be inhibited by it at all! Right?

Well…maybe…but there’s still the issue of estrogen caused by that HCG-stimulated surge in testosterone. Well…we can use low doses (300iu or so) to avoid some of that major spike in estrogen, and thus cause far less inhibition from the HCG (26). Of course, I’d want to use a bit more HCG per injection (500iu), if I could, to get my body functioning fully more quickly, and lose less of my gains. Maybe we can get away with taking some Vitamin E with our HCG, since it increases the responsiveness of plasma testosterone levels to HCG, making them significantly higher during vitamin E administration than without it (27). So we can get a better
response with our HCG by taking Vitamin E (I recommend 1,000iu/day), but that doesn’t get rid of the problem that we have, which is the estrogen increase the HCG will cause.

Lets solve that pesky estrogen problem now….

Lets add in an Aromatase Inhibitor! Which one, though? Well, since we are already using Nolvadex, we can’t use Letrozole or Arimidex, as the Nolvadex will actually greatly decrease the blood plasma levels of them (28)!

So we have to use Aromasin (exemestane) as our AI, because it’s an aromatase inactivator, meaning it makes estrogen receptors useless, and instead of just inhibiting production (as an anti-aromatase would do) it cuts off production totally. Aromasin can also cause androgenic sides (29)(30)(31), which may help to elevate your mood while you are on PCT. This final drug in my recommended PCT can effectively remove up to about 85%+ of estrogen from your body (32). Most importantly, using Aromasin together with Nolvadex doesn’t reduce exemestane’s effectiveness (33). So now, I think the problem of ANY inhibition possible with HCG is solved, and we can use that 500iu/day dose that I wanted to use previously.

With this PCT, there will be a rapid increase in LH, FSH, and testosterone, as well as almost a complete block on all the factors that could be causing your natural hormones to be delayed in returning to baseline. For this reason, I feel that the second your cycle is over is when you should start this PCT (a week after your last shot, or the day after your last pill is fine). Remember, waiting for some of the extra androgens you’ve been taking to leave your body is nonsensical, as we want to start recovery as soon as possible to retain maximum gains. There is no evidence to suggest waiting any length of time after your cycle is over will increase PCT effectiveness…it simply prolongs the time you aren’t doing anything positive to regain your natural hormones. And how long do we run this for? Well…we need to stop the HCG relatively soon for reasons discussed earlier. But the Nolvadex, and Aromasin can be used for awhile longer..."

Articles like that demonstrate why Anthony Roberts has been laughed off the more learned anabolic steroid discussion sites. Roberts doesn't do a PCT anyway because he is always 'on'. Taking HCG post cycle does delay recovery and taking an AI post cycle drives estrogen levels down much too low. AI's also increase the number of estrogen receptors and makes one more sensitive to the effects of estrogen. You guys should spend some time on sites like cuttingedgemuscle reading some of the archived posts by Nandi, Big Cat, Black Baccara and Ready2Explode. Those guys do know their stuff. Also read some of the old posts by SWALE on Meso-rx, one of the sites that Anthony Roberts got laughed off of.

[hugovsilva]

Dude, I understand your idea about LH suppression during PCT with hcg.
But what sense does it make to run it at the end of your cycle in order to restore testosterone production if you still have exogenous testosterone (or whatever) still suppressing you?

What I usually do is run hcg after cycling for 3 weeks at 500iu/day along with nolvadex and proviron (I prefer it to any AI) and then run the nolvadex for 1 month after finishing hcg. I'll run clen along with pct for my next cycle.

I think this way I will not be running hcg while I still have suppressing hormones in my system and after finishing hcg i'm still running volva to restore normal LH production.

[FlyByU]

I don't suggest taking HCG just towards the end of the cycle either. Ideally you should begin HCG on day one and end it when your cycle ends, or a little after depending on what compounds you have taken.
Below is the abstract that I based the idea that using 300ius of HCG eod is the optimal amount to maintain normal i.e. pre-cycle levels of ITT (intratesticular testosterone). If you take the numbers, throw them into excel, and add a trendline you'll find that 305ius eod hits baseline. This is all based on the idea that smaller, more frequent injections are better than larger amounts of HCG. If you'd like I have a few studies done on that also.
Btw, I wouldn't suggest taking proviron post cycle, because although it hasn't been found to be suppressive in eugonadal males, it will keep you suppressed for longer if you take it when in a hypogonadal state, which is what you're in post cycle. Post cycle is all about recovering the HPTA as quickly and efficiently as possible. Taking HCG during this period will delay recovery, as will taking proviron.

J Clin Endocrinol Metab. 2005 Feb 15; [Epub ahead of print] Related articles, Links


LOW DOSE HUMAN CHORIONIC GONADOTROPIN MAINTAINS INTRATESTICULAR TESTOSTERONE IN NORMAL MEN WITH TESTOSTERONE INDUCED GONADOTROPIN SUPPRESSION.

Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK, Anawalt **, Sutton PR, Wright WW, Brown TR, Yan X, Zirkin BR, Jarow JP.

Center for Research in Reproduction and Contraception, Geriatric Research Education and Clinical Center, Veteran Affairs Puget Sound Health Care System (AMM), and Department of Medicine, University of Washington School of Medicine (ADC, WJB, JKA, **A, PLS), Seattle, WA; Department of Medicine, Charles R. Drew University (KLH), Los Angeles, CA; Department of Urology, Johns Hopkins University School of Medicine (XY, JPJ), Baltimore, MD; Division of Reproductive Biology, Department of Biochemistry and Molecular Biology Johns Hopkins University School of Public Health (WWW, TRB, XY, BRZ, JPJ), Baltimore, MD.

In previous studies of testicular biopsy tissue from healthy men, intratesticular testosterone (ITT) has been shown to be much higher than serum testosterone (T), suggesting that high ITT is needed relative to serum T for normal spermatogenesis in men. However, the quantitative relationship between ITT and spermatogenesis is not known. To begin to address this issue experimentally we sought to determine the dose response relationship between human chorionic gonadotropin (hCG) and ITT to determine the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 mg T enanthate (TE) weekly in combination with either saline placebo or hCG 125 IU, 250 IU, or 500 IU every other day for 3 weeks. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and the end of treatment. Baseline serum T (14.1 nmol/L) was 1.2% of ITT (1174 nmol/L). LH and FSH were profoundly suppressed to 5% and 3% of baseline respectively, and ITT was suppressed by 94% (1234 nmol/L to 72 nmol/L) in the TE/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Post-treatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain normal steroidogenesis in men.

[hugovsilva]

Ideally you should begin HCG on day one and end it when your cycle ends, or a little after depending on what compounds you have taken.

This was really interesting read, thank you for posting this.

But there is 1 thing in which I disagree with you:
1-This study was performed for 3 weeks only and as you must know, prolongued use of hcg downregulates LH-receptors in the Leydzig cells. That's why most don't run it all cycle long.

This study refers to raising ITT levels, not serum T levels. You can make that association, but in this study there is no evidence that raising ITT would raise serum T.

Could you pm me your links on this hcg in (or not) in pct?

Thanks again

As for the proviron, you may be right but since it is a steroid, but I remember reading the opposite.

[FlyByU]

This was really interesting read, thank you for posting this.

But there is 1 thing in which I disagree with you:
1-This study was performed for 3 weeks only and as you must know, prolongued use of hcg downregulates LH-receptors in the Leydzig cells. That's why most don't run it all cycle long.

This study refers to raising ITT levels, not serum T levels. You can make that association, but in this study there is no evidence that raising ITT would raise serum T.

Could you pm me your links on this hcg in (or not) in pct?

Thanks again

As for the proviron, you may be right but since it is a steroid, but I remember reading the opposite.

I would not consider a 10-12 week run of HCG a long course and in low doses, it has never been shown in any study to cause damage to the leydig cells. Dr John Crisler (SWALE) who used to post regularly on the men's health board on Meso-rx has all his TRT guys on low doses of HCG so that they are never completely shut down - one very important part of the HPTA (the leydig cells in the testes), is still very much active.
Post cycle, the main opposition to recovery is poor testicular function. If the testes have been dormant all cycle, recovery will take much longer. Taking HCG from the beginning of the cycle in the correct dose, stimulates the leydig cells to produce as much testosterone as they do under normal (eugonadal) circumstances, so that post cycle you don't have to play "catch up" in regard to restoring testicular function.
The study is referring to ITT levels, specifically maintaining normal (eugonadal) levels of ITT. If the leydig cells are still producing testosterone during a cycle, of course serum levels will be higher. When HCG is not used during a cycle, there will be no testosterone released by the leydig cells after a short time, because there is no LH to stimulate its release.

[hugovsilva]

Anyway I don't think its worth taking chances of LH receptor downregulation, to cut your body's response to hcg when you need it the most-after cycle.

That's why I think it should be ran 2-3 weeks mid cycle (in my case 12 weeks so I will run it week5-7), and then after cycle along with nolvadex, being that nolvadex should be continued for an extra 3 or 4 weeks.

You keep yours and I keep mine.