HCG - The 2 schools of thought

[Drummer]

Just seeing a lot of people asking about HCG, So making this thread for an easy search and read. HCG is a replacement for your natural LH - LH drops off when you cycle and thats when your balls are told to shut down. If this is for an extended period of time, your balls will likely shrink, and will have to grow back later. This can take several months, and is associated with the "crash" many people experience. HCG is used to replace that LH. It must be used wisely, because high doses can desensitize your boys and render them forever less productive.

There are 2 main schools of thought regarding the use of HCG. Some say use it at the end of a cycle while the juice is clearing your system, right before your PCT. At this point, your boys may be very shrunken. Some say use it during a cycle. This is to help prevent the boys from shrinking in the first place. Both schools of thought have people saying it worked for them... but IMHO, one is much better than the other. If you have tried both ways, you may be able to back me up here.

If you are doing a cycle that will shut you down and cause atrophy(shrinkage) you already know it takes a while to grow the boys back, even with HCG. During this time you may become weaker, lethargic, and find it harder to get to the gym. You may lose some of your gains. Many of us can overcome this mentally, but its still an effort.

For this reason I believe that taking HCG during a cycle and ending it as the last esters run out of your body is the best method. Then you can start your proper PCT. At this point you should have maintained the size of your boys and should be able to get back to homeostasis (hormonal balance) quicker during PCT. Another benefit of running HCG with your cycle is the addition of natural testosterone. Your boys will be being told to keep producing because of the HCG. Start the HCG right away with fast acting esters, or about 2 weeks in for long esters. End it about 4-5 days before the last ester clears your blood.

Using HCG at all depends on your cycle - a few weeks of winny is not a reason to use it. Longer cycles with suppressive compounds are a reason to use it. Most serious users are at least at that level. Even a 10 week 500mg test cycle could benefit from HCG.

When dosing at the end of a cycle, people use as much as 500iu ED or EOD for 3 weeks or so. While on cycle, the doses can be lower, somewhere around 100-150iu ED, on average. You can take it ED or add up 3 days and take it E3D (e.g. 300iu E3D). It is usually sold in 5000iu amps, one powder and one BA. Once mixed, it must be refrigerated and used in a few weeks. I like to preload several insulin needles for sub-q injection, or several 27's for IM injection. Dont forget, HCG will also add to the overall test levels, so keeping an eye on your estrogen is still important, and all the same rules apply for estrogen control.

So there you have it, a short simple explanation of typical HCG usage. Your welcome :tu

~D~

[Solo59]

Good information, and clearly expressed!

Solo

[gustavo77]

Good post bro...very much along the lines of what i recommend...

I do think though that HCG can be used too frequently...shots taken every 3-4 days is optimal. Shot taken any closer together, say ED or EOD can cause over-stimulation and actually damage the leydig cells of the testes. HCG causes peak output of the testes in 48-72hrs.. I have actually read that the testes respond best to this type of "pulse" dosing, every 3-4 days, as it mimics the body's own release of LH. Not sure how accurate that is but every 3-4 day dosing on cycle has worked well for me...even at my age...haha..

[punkrock]

Good post bro...very much along the lines of what i recommend...

I do think though that HCG can be used too frequently...shots taken every 3-4 days is optimal. Shot taken any closer together, say ED or EOD can cause over-stimulation and actually damage the leydig cells of the testes. HCG causes peak output of the testes in 48-72hrs.. I have actually read that the testes respond best to this type of "pulse" dosing, every 3-4 days, as it mimics the body's own release of LH. Not sure how accurate that is but every 3-4 day dosing on cycle has worked well for me...even at my age...haha..

What do you guys think would be the lowest effective or lowest safe dosage for bi weekly injections? And what kind of dose would you take yourself?

I've only done post cycle hcg.

[Drummer]

Good post bro...very much along the lines of what i recommend...

I do think though that HCG can be used too frequently...shots taken every 3-4 days is optimal. Shot taken any closer together, say ED or EOD can cause over-stimulation and actually damage the leydig cells of the testes. HCG causes peak output of the testes in 48-72hrs.. I have actually read that the testes respond best to this type of "pulse" dosing, every 3-4 days, as it mimics the body's own release of LH. Not sure how accurate that is but every 3-4 day dosing on cycle has worked well for me...even at my age...haha..

Even though i wasnt aware of this, it sounds legit. If a pulse is closer to how our bodies operate, i would go with that. 300iu E3D sounds pretty good, on cycle.

~D~

[Ritch]

Say you pin twice a week because you`re using long esters, but hear about pinning hcg E3D. At some point you will pin the hcg on the same day you take a shot. Something I heard is not good. So if you were to pin hcg twice a week and pin your stroids twice a week, would it not be best to pin the hcg the day before your shot?

Example. You pin steroids on Sunday and Wednesday, hch shot every tuesday and saturday.

[gustavo77]

What do you guys think would be the lowest effective or lowest safe dosage for bi weekly injections? And what kind of dose would you take yourself?

I've only done post cycle hcg.

250-500iu 2x per week is a good dose...i take between 500 and 1000iu to be honest...mostly 500iu...sometimes if i miss a shot or two or run out of HCG for a week or two, I will take 1000iu at once...i do not go over 1000iu though...some people do but i like to err on the side of caution with stuff like this.

[gustavo77]

Say you pin twice a week because you`re using long esters, but hear about pinning hcg E3D. At some point you will pin the hcg on the same day you take a shot. Something I heard is not good. So if you were to pin hcg twice a week and pin your stroids twice a week, would it not be best to pin the hcg the day before your shot?

Example. You pin steroids on Sunday and Wednesday, hch shot every tuesday and saturday.

I know there are some on the board who have HCG & test prescribed for them and their docs have a specific protocol for when to take HCG in relation to test shots...myself, i figure as long as i get 1-2 shots in of HCG per week, i am good shape testes wise...lol...but i would like to hear some further comment on this...

[Ritch]

I know there are some on the board who have HCG & test prescribed for them and their docs have a specific protocol for when to take HCG in relation to test shots...myself, i figure as long as i get 1-2 shots in of HCG per week, i am good shape testes wise...lol...but i would like to hear some further comment on this...

Looking forward to hearing this as well. I think somebody was saying he was on trt doses and would take the hcg 2 days in row followed by his test shot.

[Drummer]

Say you pin twice a week because you`re using long esters, but hear about pinning hcg E3D. At some point you will pin the hcg on the same day you take a shot. Something I heard is not good. So if you were to pin hcg twice a week and pin your stroids twice a week, would it not be best to pin the hcg the day before your shot?

Example. You pin steroids on Sunday and Wednesday, hch shot every tuesday and saturday.

Personally i never think in terms of shots per week because a week is uneven in days. I always think in terms of how many days apart each shot is. So, e3d will end up being 2x one week, 3x the next etc. If taking the hcg in relation to the aas is a concern, i would just stagger the shots myself. But i have not heard of it being bad nor can i think of a reason. However, im open to the idea...


I always plan cycles like this :

250mg test EOD for 84 days (12 weeker) etc.


~D~

[canadianmuscle0803]

great post bro..

this is a stupid question, but i never once claimed to be a smart guy..

i only have 5,000iu vials and i like to take my HCG during my cycles.. the vials are 2ml, so i can add 2ml bac water.. what number should i go to on the slin needle for my injections? i mean if i only need 500iu E3D and 1ml is 2,500iu, 500 would be 1/5th of that ml right? wtf is 1/5th of the slin needle? its early in the morning and i havent slept, i swear im not usually this dumb.. i have been going up to the number 20 on the slin pin so far.. whos goog in math? how many IUs that does work out to? is that 1/5th lol..

[BAM]

^^
2ml / 5000iu

2500iu / ml

1250iu / 1/2 ml

625iu / 1/4 ml (25 on a 1/2 ml slin pin)

625ui / 25 notches = 25iu per notch

So yes.. 20 on he slin pin is correct for 500iu in your scenario


but... the powder adds slightly to the liquid volume
so it might actually be 21 notches for 500iu. I never actually measured how much
the volume of liquid is affected by the powder

[canadianmuscle0803]

thanks Bam.. i figured i was right but like i said im fuzzy this morning.

[Ritch]

I have a tough time with math myself just remember:


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[Drummer]

^^^^ lol

[waderow]

there is actually three trains of thought.


HCG/Nolva/Clomid for PCT.

[punkrock]

So if you pin HCG during your cycle. What should your pct look like? HCG at high volume still, not at all, or just that same as you have throughout the cycle?

[Drummer]

HCG is suppressive itself, so I cant see any good reason to use it for PCT. Some people call it PCT also, but that protocol almost always stops the HCG a few weeks before the serm/AI (nolva, aromasin for e.g.). It makes no sense to run HCG to the end of the PCT as it suppresses natural LH.

~D~

[waderow]

HCG is suppressive itself, so I cant see any good reason to use it for PCT. Some people call it PCT also, but that protocol almost always stops the HCG a few weeks before the serm/AI (nolva, aromasin for e.g.). It makes no sense to run HCG to the end of the PCT as it suppresses natural LH.

~D~

The only medically proven form of PCT involves HCG, Nolva and clomid

[waderow]

copy and pasted:

Default The Proper PCT Protocol and Why
I've seen a lot of questions lately regarding the proper PCT. There is a lot of info available, so if people do their research, then they will find answers. The problem is, there are so many various answers. I just read a post where someone recommends using Proviron during PCT. The problem with this is that Proviron is a mild androgen, and will keep you shut down. Here is the proper PCT protocol. If I see another question about proper PCT after I take the time to type all this out, then I am going to pull my hair out!!!

This information is taken from Anabolics 2007 by William Llewellyn, but put into easy-to-understand terms for the newbies out there.

BACKGROUND

When you take AAS, your body stops making natural hormones (i.e., test). Once you stop taking steroids, you can be left with a gap until your body starts making its own again, which can take months. Here, you can be faced with low levels of androgens and normal levels of corticosteroids. Corticosteroids have a pronounced catabolic (muscle-depleting) state on our bodies, and without the androgens to balance the catabolic effects of corticosteroids, a good deal of your new muscle mass may be lost. To help your body maintain its size, you will want to restore endogenous (natural) testosterone production quickly. The methods for doing this seem to be different everywhere you look: "Take hCG, don't take hCG, use an aromatase inhibitor, just take Clomid, forget Clomid and just take Nolvadex." What option is reall best? Without an understanding of what is really happeningin your body, and why certain compounds help to correct the situation, choosing he correct PCT program can be quite confusing.

The HPTA Axis

The Hypothalamic-Pituitary-Testicular Axis (HPTA) is the thermostat for your body's natural production of testosterone. Too much testosterone, and the furnace will shut off. Not enough, and the heat is turned up (to put it very simply). For the purpose of our discussion, we can look at this regulating process as having three levels. At the top is te hypothalamic region of the brain, which releases the hormone GnRH (Gonadotropin-Releasing Hormone) when it senses a need for more testosterone. GnRH sends a signal to the second level of the axis, the pituitary, which releases Luteinizing Hormone in response. LH for short, this hormone stimulates the testes (level three) to secrete testosterone. The same sex steroids (testosterone, estrogen) that are produced serve to counterbalance things, by providing negative feedback signals (primarily to the hypothalamus and pituitary) to lower the secretion of testosterone. Synthetic steroids send the same negative feedback. This quick background of the testosterone-regulating axis is necessary to furthering our discussion, as we need to first look at the underlying mechanism involved before we can understand why natural recovery of the HPTA post-cycle is a slow process. Only then can we implement an ancillary drug program to effectively deal with it.

Testicular Desensitization

Although steroids supress testosterone production primarily by lowering the level of gonadotropic hormones, the big roadblock to a restored HPTA after we come off steroids is surprisingly not LH. This problem was made clearly evident in a study published back in 1975. Here, blood parameters, including testosterone and LH levels, were monitored in male subjects who were given testosterone enanthate injections of 250mg weekly for 21 weeks, a low dose for even a beginner's cycle. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which was to be expected. Things looked very different, however, once the steroids had been withdrawn. LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average, it was more than 10 weeks before any noticeable movement in testosterone production started at all! This lack of correlation makes clear that the problem in getting androgen levels restored is not necessarily the level of LH, but more so testicular atrophy and desensitization to LH. After a period of inactivation, the testes have lost mass (atrophied), making them unable to perform the required workload. The protracted post-cycle window can, likewise, no longer be looked at as one of low testosterone and low LH. Much of it actually involves low testosterone and normal (even high) LH.

The Role of Anti-Estrogens

It is important to understand that anti-estrogens alone are inadequate to restore normal endogenous testosterone production after a cycle. These agents ordinarily increase LH levels by blocking the negative feedback of estrogens. But LH rebounds quickly on its own post-cycle, without help. Plus, there is not an elevated level of estrogen for anti-estrogens to block during this window, as testosterone (now suppressed) is a major subtrate used for the synthesis of estrogen in men. Serum estrogen levels are actually lower here, not higher. Any estrogen rebound that occurs post-cycle, likewise, happens with a rebound in testosterone levels, not prior to it (there is an imbalance in the ratio of androgens to estrogens post cycle, but this is another topic altogether). On their own, we are seeing no mechanism in which anti-estrogenic drugs can effectively help here. I can, however, see why this fact would be easy to overlook. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels in men, and in normal situations they indeed perform this function very well. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that we need to focus on LH. We would miss the true problem, testicular desensitization, unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in focusing solely on anti-estrogenic drugs.

The Role of hCG

With anti-estrogens alone proving to be ineffective, we are left to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this, we will need the injectable drug hCG. If you are not familiar, hCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the body's natural LH. Although the testes are equally desensitized to this drug as they are to LH (they work through the same receptor), we are administering it as a measured drug and are, therefore, not constrained by the limits of our own LH production. In other words, we can give ourselves a good dose of the drug (as much LH as we really need), shocking the testes with unnaturally high levels of stimulation. We want it to reach a level above what our bodies, even when supported by anti-estrogens, could do on its own. The result should be a more rapid restoration of original testicular mass, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program in place. What we are looking at now is hCG actually being the pivotal post-cycle drug, with anti-estrogens playing more of a supportive role.

The PoWeR PCT Program

The PCT program outlined below represents what I consider to be an ideal and effective PCT program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover from abnormal hormonal functioning following steroid therapy. One of the key doctors on this program, Dr. Michael Scally, claims to have successfully treated more than 100 cases of hypogonadism/hypogonadotropic hypogonadism, and is very well known in the field of androgen replacement therapy. PoWeR published this program as part of a recent clinical study, which involved 19 healthy male subject who were taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks. Their HPGA Normalization Protocol focuses on the combined use of hCG, Nolvadex, and Clomid, and is perhaps the only clinical documented post-cycle therapy program to be found in the medical literature (it is amazing how little attention has been paid to hormone normalization in clinical medicine). The most notable variation from a classic PCT stack, such that I have been a longtime supporter of, is the combined use of two anti-estrogens. In this case I cannot say there is a disadvantage to such us; perhaps it is indeed the better option.

NOLVADEX: ran for 45 days from day 1
CLOMID: ran for 30 days from day 1
hCG: ran for 16 days from day 1

Examining the program closely, we note that the testes are hit hard with hCG at the onset of therapy. Its intake, however, is limited to only 16 days. The doctors undoubtedly recognize that when hCG is taken for too long or at too high a dosage it can desensitize the LH receptor. This would only further exacerbate the post-cycle program, not help it. Anti-estrogens are used during and after hCG, with a dosage of 10mg of Nolvadex and 100mg of Clomid per day, rounding out this compliment of drugs. Clomid is used for a shorter period of time than Nolvadex, likely because of the desensitizing effect it too can have (on the pituitary gland) with continued use. Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start to go back up, as well as combat any potential estrogenic side effects that may be caused by hCG's up-regulation of testicular aromatase activity. Although the first couple of weeks the anti-estrogens probably do very little, they should be much more helpful toward the middle and end of the program. During this clinical investigation, normal hormonal function was restored in all subjects within 45 days of drug cessation. This is a definite success, far more favorable than the protracted recovery window noted in studies without PCT, such as the 250mg/week testosterone enanthate investigation. Such a detailed recovery program should follow any serious steroid cycle. It is the best way to maintain your gains at their maximum, and that is, after all, what we are after.

PRACTICAL APPLICATION

After having read this, I have applied this to my PCT program. I have chosen to run hCG at 1500iu on day 1, 1500iu on day 5, and 1500iu on day 9. Also, I have chosen to run Clomid for 21 days versus 30 days, in an effort to not desensitize my pituitary, and the dose is 100mg/day for the first 7 days, then 50mg/day for the next 14 days. In addition, I decided to run the Nolvadex for the full 45 days. I run 40mg/day the first week, 30mg/day the second week, 20mg/day the third week, and 10mg/day weeks four through six. After having ran my PCT like this after three cycles, and then having my testosterone levels checked after each PCT, I have found that my levels have returned to the normal range, as expected.

hCG: 1500iu E4D, 3 doses total, from day 1
Week 1: Nolva 40mg/day; Clomid 100mg/day
Week 2: Nolva 30mg/day; Clomid 50mg/day
Week 3: Nolva 20mg/day; Clomid 50mg/day
Week 4-6: Nolva 10mg/day

[waderow]

HYPOTHALAMIC PITUITARY GONADAL AXIS NORMALIZATION PROTOCOL AFTER ANDROGEN TREATMENT

Antiviral Therapy 2002; 7:L53 (abstract 81)

N Vergel1, AL Hodge2, MC Scally3
1Program for Wellness Restoration, PoWeR, Houston, Texas; 2University of Houston Department of Exercise Science, Houston, Texas; 3MDMuscle Houston, Texas

OBJECTIVE: To develop an approach to cycle androgens that would result in significant changes in body composition and accelerate the normalization of the hypothalamic pituitary gonadal axis (HPGA) after cessation of androgens.

METHODS: An uncontrolled study of 19 HIV-negative eugonadal men, ages 23–57 years, administered testosterone cypionate and nandrolone decanoate for 12 weeks, and then were treated simultaneously with a combined regimen of human chorionic gonadotropin (hCG) (2500 IU/four times daily ×16 days), clomiphene citrate (50 mg PO twice daily ×30 days) and tamoxifen (20 mg PO once daily ×45 days), to restore the HPGA.

RESULTS: Mean FFM by DEXA increased from 64.1 to 69.8 kg (P<0.001); percent body fat decreased from 23.6 to 20.9 (P<0.01); strength increased significantly from 357.4 lb to 406.4 lb (P=0.02). No significant changes in serum chemistries and liver function tests were found. HDL-C decreased from a mean value of 44.3 to 38.0 (P=0.02). Mean values for luteinizing hormone (LH) and total testosterone were 4.5 and 460, respectively, prior to androgen treatment. At the conclusion of the 12-week treatment with androgens the mean LH <0.7 (P<0.001) and total testosterone was 1568 (P<0.001). The mean values after treatment with the combined regimen were LH=6.2 and testosterone=458.

DISCUSSION: The use of androgens has been reported to improve lean body mass, strength, sexual function, and mood, accompanied by side-effects caused by continuous uninterrupted use of these compounds (polycythemia, testicular atrophy, hypertension, liver dysfunction [oral androgens] and alopecia). Androgeninduced HPGA suppression causes a severe hypogonadal state in most patients that often require an extensive period of considerable duration for normalization. This prevents most if not all individuals from cycling off these medications due to the adverse impact of this state on their previously gained LBM and quality of life. The protocol of hCG-clomiphene-tamoxifen was successful in restoring the HPGA within 45 days after androgen cessation. Further controlled studies are needed to determine if these results can be duplicated in HIV-positive subjects.

Presenting author: N Vergel

[Drummer]

^^ i havent had time to read it all, but by looking at the end protocol, I think i know who wrote it, and its the same as what i've said. HCG stops before the serms and AI. Good posts to have in this thread tho,

~D~

[waderow]

and its the same as what i've said. HCG stops before the serms and AI

~D~

correct, but is still the main part of the PCT

[waderow]

^^ i havent had time to read it all, but by looking at the end protocol, I think i know who wrote it, and its the same as what i've said. HCG stops before the serms and AI. Good posts to have in this thread tho,

~D~

post 21 is the real protocol

[deleteduser0002]

HCG 2500iu's/ 4 times daily for 16 days! Wow, thats a lot of HCG!

[canadianmuscle0803]

HCG 2500iu's/ 4 times daily for 16 days! Wow, thats a lot of HCG!

what, where, how? wtf.. who said this?

[waderow]

what, where, how? wtf.. who said this?

N Vergel1, AL Hodge2, MC Scally3
1Program for Wellness Restoration, PoWeR, Houston, Texas; 2University of Houston Department of Exercise Science, Houston, Texas; 3MDMuscle Houston, Texas

[gustavo77]

So if you pin HCG during your cycle. What should your pct look like? HCG at high volume still, not at all, or just that same as you have throughout the cycle?

HCG is not needed during pct if used on cycle....what i suggest for pct:

Wk 1-3 Clomid 50-100mg/day
Wk 1-5 Aromasin 25mg/day

[deleteduser0002]

HCG is not needed during pct if used on cycle....what i suggest for pct:

Wk 1-3 Clomid 50-100mg/day
Wk 1-5 Aromasin 25mg/day

Curious...why is aromasin run longer than clomid? If the aromasin "kills" estrogen than estrogen rebound wouldn't be a concern after all AAS have left your system (would it?)

[gustavo77]

HYPOTHALAMIC PITUITARY GONADAL AXIS NORMALIZATION PROTOCOL AFTER ANDROGEN TREATMENT

Antiviral Therapy 2002; 7:L53 (abstract 81)

N Vergel1, AL Hodge2, MC Scally3
1Program for Wellness Restoration, PoWeR, Houston, Texas; 2University of Houston Department of Exercise Science, Houston, Texas; 3MDMuscle Houston, Texas

OBJECTIVE: To develop an approach to cycle androgens that would result in significant changes in body composition and accelerate the normalization of the hypothalamic pituitary gonadal axis (HPGA) after cessation of androgens.

METHODS: An uncontrolled study of 19 HIV-negative eugonadal men, ages 23–57 years, administered testosterone cypionate and nandrolone decanoate for 12 weeks, and then were treated simultaneously with a combined regimen of human chorionic gonadotropin (hCG) (2500 IU/four times daily ×16 days), clomiphene citrate (50 mg PO twice daily ×30 days) and tamoxifen (20 mg PO once daily ×45 days), to restore the HPGA.

RESULTS: Mean FFM by DEXA increased from 64.1 to 69.8 kg (P<0.001); percent body fat decreased from 23.6 to 20.9 (P<0.01); strength increased significantly from 357.4 lb to 406.4 lb (P=0.02). No significant changes in serum chemistries and liver function tests were found. HDL-C decreased from a mean value of 44.3 to 38.0 (P=0.02). Mean values for luteinizing hormone (LH) and total testosterone were 4.5 and 460, respectively, prior to androgen treatment. At the conclusion of the 12-week treatment with androgens the mean LH <0.7 (P<0.001) and total testosterone was 1568 (P<0.001). The mean values after treatment with the combined regimen were LH=6.2 and testosterone=458.

DISCUSSION: The use of androgens has been reported to improve lean body mass, strength, sexual function, and mood, accompanied by side-effects caused by continuous uninterrupted use of these compounds (polycythemia, testicular atrophy, hypertension, liver dysfunction [oral androgens] and alopecia). Androgeninduced HPGA suppression causes a severe hypogonadal state in most patients that often require an extensive period of considerable duration for normalization. This prevents most if not all individuals from cycling off these medications due to the adverse impact of this state on their previously gained LBM and quality of life. The protocol of hCG-clomiphene-tamoxifen was successful in restoring the HPGA within 45 days after androgen cessation. Further controlled studies are needed to determine if these results can be duplicated in HIV-positive subjects.

Presenting author: N Vergel


Wow...that's a lot of HCG...

As i said in my above post, HCG used on cycle at moderate doses will negate the need for HCG (at crazy doses i might add) to kick start the testes during PCT.

When you use HCG on cycle, the TA part of the HPTA is always working...all you need to do during pct is stimulate the HP or Pituitary secretion of LH AND also, keep estrogen under control...

Yes the protocol in the above study worked...of course it did...HCG and SERM overload... but that does not mean it is the most effective and efficient.

[gustavo77]

Curious...why is aromasin run longer than clomid? If the aromasin "kills" estrogen than estrogen rebound wouldn't be a concern after all AAS have left your system (would it?)

Nope...the great thing about aromasin is that there is NO estrogen rebound....aromasin destroys the aromatase enzyme...so once aromasin use is ceased it will take time for the body get enzymes back to normal levels, so estrogen production will resume gradually...

[waderow]

Yes the protocol in the above study worked...of course it did...HCG and SERM overload... but that does not mean it is the most effective and efficient.

That doesnt mean it isnt the most effective and efficient PCT protocol either.

It could very well be the best PCT protocol on earth, but to date, the ONLY documented PCT protcol by medical study, and documented to work well I might add.
All other PCT protocols are bro science. Work? yes. Sure they do, tried tested and true. As good as this? probably not, but who knows

[Praetorian]

HCG is not needed during pct if used on cycle....what i suggest for pct:

Wk 1-3 Clomid 50-100mg/day
Wk 1-5 Aromasin 25mg/day

I would have to disagree with that. HCG is definitely needed even if run during the cycle depending on the individual. You cannot generalize things this way at all.
Even if used at a low dose 500iu per day for a couple days on cycle will not be enough for some to recover on clomid alone. Ive seen this first hand on many BB's it just doesnt work. Guys seem to think a dosage over 500iu is going to damage leydig cells etc...this is just not the case. The manufacturer of Canadian Pharmaceutical grade HCG suggests the dosage for hypogonadal men as 4000-5000iu 3-4 times weekly for 6 weeks.
P

[Praetorian]

Another study:

HPTA reversal using HCG+Clomid+Tamoxifen

Objective:
Although shown to be effective for their intended medical treatment, AAS have been shown to induce hypogonadotropic hypogonadism in adult males. The medical literature is conflicting in the reports of spontaneous return and long-term suppression of gonadal suppression post AAS usage. This observational study documents the treatment protocol of HCG, clomiphene citrate, and tamoxifen in returning hormonal function to normal post AAS usage. Design:
Five HIV-negative males age 27-49, weighing 77-100 kg, with serum total testosterone levels below 240 ng/dL and luteinizing hormone (LH) levels below 1.5 mIU/mL were considered for this observational study. All five patients were administered the treatment protocol.
Methods:
Treatment consisted of combination therapy which included concurrent administration of (a) Human Chorionic Gonadotropin, (b) Clomiphene Citrate and (c) Tamoxifen Citrate for a standard duration of 45 days. This protocol was repeated with every patient until serum LH and total testosterone values reached normal ranges.
Results:
All five patients were considered eugonadal by normal laboratory reference ranges by the conclusion of treatment. Average serum total testosterone rose from 98.2 to 692.8 ng/dL (p<.001) while the average serum LH rose from an average undetectable value of less than 1.0 to 7.92 mIU/mL (p<.0008).

Conclusions: Although the treatment protocol of HCG, clomiphene citrate, and tamoxifen proved beneficial in reversing AAS induced hypogonadotropic hypogonadism, future controlled studies need to be performed to confirm the beneficial effects of this combined pharmacotherapy in returning HPGA functioning to normal.
Key Words- anabolic-androgenic steroids, clomiphene, HCG, tamoxifen, testosterone, HIV

INTRODUCTION
Testosterone and testosterone analogues, anabolic-androgenic steroids
(AAS), have long been used in the athletic community for improving lean muscle tissue and strength. A positive correlation has been shown with testosterone to include:
increased protein synthesis resulting in lean muscle tissue development (Bhasin et al, 1996; 1997; Hervey et al, 1981; Tenover, 1992),
enhanced sexual desire (libido) (Schiavi et al, 1991),
increased muscular strength (Bhasin et al, 1996; 1997; Hervey et al, 1981; Sih et al, 1997),
increased erythropoiesis (Bhasin et al, 1997; Evans & Amerson, 1974; Sih et al, 1997; Tenover, 1992),
a possible positive effect on bone development (Anderson et al, 1996; 1997; Baran et al, 1978; Tenover, 1992),
improved mental cognition and verbal fluency (Alexander et al, 1998), and male masculinizing characteristics (Starr & Taggart, 1992).

Recently, however, clinicians have recognized the potential benefits of their use in the treatment of various disorders and ailments. Numerous studies have discussed the use of AAS in the treatment of HIV-associated conditions (Bhasin et al, 2000; Grinspoon et al, 1998; 1999; 2000; Rabkin et al, 1999; 2000; Sattler et al, 1999; Strawford et al, 1999; Van Loan et al, 1999), hypogonadism (Bhasin et al, 1997; Davidson et al, 1979; Rabkin et al, 1999; Sih et al, 1997; Snyder et al, 2000; Tenover, 1992; Wagner & Rabkin, 1998; Wang et al, 2000), impotence (Carani et al, 1990; Carey et al, 1988; Klepsch et al, 1982; Lawrence et al, 1998; McClure et al, 1991; Morales et al, 1994; 1997; Nankin et al, 1986 Rakic et al, 1997; Schiavi et al, 1997), burn victims (Demling et al, 1997), various anemia’s (Doney et al, 1992; Gascon et al, 1999; Hurtado et al, 1993; Stricker et al, 1984), deteriorated myocardium (Tomoda, 1999), glucose uptake (Hobbs et al, 1996), continuous ambulatory peritoneal dialysis (CAPD) (Dombros et al, 1994), alcoholic hepatitis (Bonkovskyet al 1991; Mendenhall et al, 1993), hemochromatosis (Kley et al, 1992) and prevention of osteoporosis (Anderson et al, 1996; 1997; Baran et al, 1978; Behre et al 1997; Hamdy et al, 1998; Prakasam et al, 1999).
While AAS have proven effective in cases of lean muscle wasting conditions (HIV/AIDS), this class of medicines is not without their inherent problems. AAS have been shown to induce hypogonadotropic hypogonadism (Alen et al, 1987; Bhasin et al, 1996; Bijlsma et al, 1982; Clerico et al, 1981; Jarow & Lipshultz, 1990; Strawford et al, 1999; Stromme et al, 1974). This condition typically results from an abnormality in the normal functioning of the hypothalamic-pituitary-gonadal axis (HPGA), usually from a negative feedback inhibition of one of the hormone secreting glands, causing a cascading unbalance in the rest of the axis. Possibly resulting from a physiological abnormality (i.e. mumps orchitis, Klinefelters syndrome, pituitary tumor) or as an acquired result of exogenous factors (i.e. androgen therapy, AAS administration). Clerico et al (1981) found a dramatic suppression of serum gonadotropin levels in athletes given methandrostenelone, suggesting a direct action of AAS on the hypothalamus. Similar results of suppressed gonadotropins have been found in patients supplementing solely testosterone (Bhasin et al, 1996; Marynick et al, 1979; Strawford et al, 1999; Tenover, 1992). Case report studies discussed a 36-year old male competitive bodybuilder and a 39-year old father, each using various AAS regimens over extended periods of time, who showed a blunted response to GnRH stimulation tests (Jarow & Lipshultz, 1990). One particular study administered 600 mg of nandrolone decanoate to 30 HIV-positive males over twelve weeks (Sattler et al, 1999). The results made no reference to LH or testosterone levels. The lack of gonadotropin measurement is puzzling as the data showed 12 of 30 subjects experienced testicular shrinkage, implying Leydig cell dysfunction and suppressed testosterone levels. Other studies using AAS have also shown no reference to LH or FSH levels but suppressed values are expected in each case (Bagatell et al, 1994; Behre et al, 1997; Sheffield-Moore et al, 1999; Tricker et al, 1996).
Declining, or suppressed, circulating testosterone levels as a result of either pathophysiological or induced hypogonadal conditions can have many negative consequences in males. Declining levels of testosterone have been directly linked to a progressive decrease in muscle mass (Mauras et al, 1998), loss of libido (Schiavi et al, 1991), decrease in muscular strength (Balagopal et al, 1997; Mauras et al, 1998) impotence (Rakic et al, 1997), oligospermia or azoospermia (Vermeulen & Kaufman, 1995), increase in adiposity (Mauras et al, 1998) and an increased risk of osteoporosis (Wishart et al, 1995).
While some research suggests that the hormonal axis will spontaneously return to normal shortly after cessation of testosterone administration (Knuth et al, 1989), documented cases have taken up to 2 ½ years to return to normal (Jarow & Lipshultz, 1990). This case of a 39-year old male who previously used AAS was found to have low serum testosterone levels (6nmol/L, range 14 to 28 nmol/L) 2 ½ years after his last administration of the drugs (Jarow & Lipshultz, 1990). For most men, suffering with diminished libido, impotence, depression, fatigue, muscle atrophy, and infertility for 2 ½ years is not a pleasant option. Other androgen or anabolic steroid induced cases of hypogonadotropic hypogonadism have taken 6 months (Gazvani et al, 1997; Wu et al, 1996), 8 months (Gazvani et al, 1997), 10 months (Boyadjiev et al, 2000), 12 months (Schurmeyer et al, 1984), and 18 months (Gazvani et al, 1997) to finally return to eugonadal status.
The individual use of human chorionic gonadotropin (HCG), clomiphene citrate, and tamoxifen citrate in the treatment of testicular sub-function and gonadotropin suppression, respectively, is well documented. HCG has been shown to significantly improve gonadal function in hypogonadotropic hypogonadal adult males (Barrio et al, 1999; Burgess & Calderon, 1997; Cisternino et al, 1998; D’Agata et al, 1982; 1984; Dunkel et al, 1985; Kelly et al, 1982; Ley & Leonard, 1985; Liu et al, 1988; Martikainen et al, 1986; Okuyama et al, 1986; Ulloa-Aguirre et al, 1985; Vicari et al, 1992). Studies using clomiphene citrate to induce endogenous gonadotropin production in males found significant improvements in LH and FSH values after treatment (Bjork et al, 1977; Burge et al, 1997; Guay et al, 1995; Landefeld et al, 1983; Lim & Fang, 1976; Ross et al, 1980; Spijkstra et al, 1988). Tamoxifen citrate has also been found to produce a profound increase in serum LH levels as well as improved semen and sperm quality (Gazvani et al, 1997; Krause et al, 1985; Lewis-Jones et al, 1987; Wu et al, 1996).
As HCG’s effect is centralized at the Leydig cells of the testicles, clomiphene citrate and tamoxifen citrate act upon the hypothalamic-pituitary region in stimulating gonadotropin production. Tamoxifen, a nonsteroidal antiestrogen, and clomiphene citrate, a nonsteroidal ovulatory stimulant, compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary and allowing gonadotropin production to resume normally. The normal operation of both the testicular and hypothalamic-pituitary regions is crucial in returning HPGA function to normal. Returning one component of the axis to normal without concurrently returning the other would sabotage and inhibit the operation of the entire HPGaxis. It was with this understanding that HCG was eventually combined with clomiphene citrate and tamoxifen as attempted therapy to reverse gonada function in hypogonadotropic hypogonadal males.
In accordance with previous studies, each medication was used individually, and along with HCG, in initial trials. The simultaneous use of clomiphene citrate and tamoxifen was determined through preliminary use of clomiphene citrate and tamoxifen individually. It was discovered that although both clomiphene citrate and tamoxifen met with some success, when combined together they achieved a more significant increase in gonadotropin production. This clinical outcome resulted in the combination therapy of HCG, clomiphene citrate and tamoxifen.

Following is a clinical evaluation of the combined, simultaneous use of HCG, clomiphene citrate, and tamoxifen citrate as a treatment option in suppressed testosterone and gonadotropin levels in hypogonadotropic hypogonadal adult males. This observational analysis of the aforementioned treatment protocol assessed the efficacy of these medicines under non-controlled conditions.

METHODS
An observational study was done on the medical records of 5 adult male patients presenting to a clinic with induced hypogonadotropic hypogonadism. Patients were monitored and treatment recorded for the purposes of this observational study.
SUBJECTS
The medical records of five males age 27-49, mean 35.2, weighing 77-100 kg, mean 89.8 kg, with serum total testosterone levels below 240 ng/dL and serum luteinizing hormone (LH) levels below 1.5 mIU/mL were examined. Average presenting testosterone level was 98.2 ng/dL (normal= 240-827 ng/dL) while average LH level was undetectable at <1.0 mIU/mL (normal= 1.5-9.3 mIU/mL). The 5 patients had a history of AAS usage ranging from 9-60 months prior to presentation. All patients had ceased any testosterone therapy or AAS usage prior to initiation of treatment. Initial laboratory values confirmed that all patients had discontinued AAS long enough for endogenous lab values to fall below normal reference ranges. All patients were muscular in nature with an average BMI less than 27 at presentation. Table 1 presents the patient characteristics, anabolic history, and side effects upon presentation of the 5 patients.

LABORATORY STUDIES
Initial blood screening consisted of:
AST, ALT, GGT, TOTAL CHOLESTEROL, LH, FSH, TESTOSTERONE, GLUCOSE, PROLACTIN, PSA TOTAL, TSH, T3 UPTAKE, T4 TOTAL, T4 FREE, HEMOGLOBIN, HEMATOCRIT
Table 2 shows all baseline serum blood levels at presentation. Baseline blood screening excluded any form of hyperprolactinemia or hypothyroidism as causes of hypogonadism in most patients. After physician examination and history and physical evaluation, it was determined that a history of AAS usage was present and most likely the cause of the patients’ hypogonadotropic hypogonadal lab values; not hyperprolactinemia or hypothyroidism.
Laboratory testing was performed by Quest Diagnostics Inc., (Houston, TX) and SmithKline Beecham Clinical Laboratories, (Houston, TX). Repeat serum LH & testosterone samples were measured by immunoassay using chiron reagant kits on an ACS-180 instrument.

METHODS
A review of patients’ medical records showed a treatment intervention of (a) human chorionic gonadotropin (HCG) (Ferring Pharmaceuticals), (b) clomiphene citrate (Teva Pharmaceuticals), and (c) tamoxifen (AstraZeneca). Typical dosage of HCG consisted of 2500 units every other day for 16 days.
All HCG injections were self-administered intramuscularly. Starting dosages of clomiphene citrate and tamoxifen were 50mg and 20 mg daily, respectively. Patients started all three medications simultaneously and reported for the first follow-up blood work after completion of HCG, 16 days later. The post HCG blood analysis assessed testosterone-total response only. If testicular stimulation, i.e. testosterone production, was inadequate, additional HCG was administered at this stage of therapy rather than waiting an additional 30-45 days before the protocol completion. If the testicular response to the HCG demonstrated sufficient testicular stimulation (typically a blood serum level of >300 ng/dL), clomiphene citrate and tamoxifen were continued for 15 and 30 days, respectively. The arbitrary cut-off level of 300 ng/dL was used as a general assessment where sufficient Leydig cell stimulation was taking place even in light of artificial stimulation from HCG. A repeat blood sample was then taken at day 45 to assess hypothalamic-pituitary-gonadal axis status via luteinizing hormone and total testosterone levels. Because of the varying cessation times of the medications, the concluding blood sample was taken after a 30 and 15-day washout period of HCG and clomiphene citrate, respectively. For HPGA function to be considered normal, both LH and testosterone values had to fall within the normal reference ranges. For the purposes of patient treatment, if LH and testosterone values were still below normal limits at the conclusion of 45 days of treatment, a repeat protocol administration of HCG, clomiphene citrate, and tamoxifen was given. This protocol was repeated with every patient until LH and testosterone values reached normal ranges.

RESULTS
All five patients were considered eugonadal by normal laboratory reference ranges by the conclusion of treatment. Average serum total testosterone rose from 98.2 to 692.8 ng/dL. Average serum LH rose from <1.0 to 7.92 mIU/mL. An average of 48,974 U of HCG (five 10,000 Unit boxes), 3412.5 mg of clomiphene citrate (68.25 50mg tablets), and 968.71 mg of tamoxifen (48.44 20mg tablets) were used to treat all patients to eugonadal. Total treatment time ranged from 43-120 days. Mean elapsed time from initiation of treatment to eugonadal was 68.6 days. Statistical analysis was performed using repeated measures ANOVA. Pre and post treatment testosterone values were significantly (p<.001) different as were the LH values (p<.0008). Table 3 demonstrates the hormone changes during the treatment period and the duration to eugonadal.

ADVERSE EVENTS
None of the study subjects had any serious or treatment-terminating effects as a result of the multi-drug protocol. No problems were noted with regards to parameters of normal urologic function or treatment causing gynecomastia. Any side effects documented at presentation were reversed by the conclusion of treatment.

DISCUSSION
This observational study demonstrates the possible efficacy of HCG, clomiphene citrate, and tamoxifen citrate in returning the HPGA to normal physiological function in adult males suffering from androgen induced hypogonadotropic hypogonadism. In the case of decreased testicular function manifested by low testosterone levels, it is of primary importance to first return the normal function of the testicular cells. The initial lack of response to HCG should not immediately be a cause for the initiation of testosterone replacement therapy, as with the current accepted therapy modality by many physicians. Blood analysis confirmed that no exogenous testosterone was administered during the treatment period, as exogenous androgens would have had a suppressive effect on endogenous gonadotropin production. Therefore, because of the corresponding normal gonadotropin and testosterone values, it is accepted that gonadotropin and testicular function were normal by the conclusion of treatment. The standard treatment of HIV-related muscle wasting, AAS therapy, may involve decades of treatment and the attendant problems with any therapy of a prolonged nature. Polycythemia vera, elevated hepatic enzymes, and prolonged negative alterations in lipid profile are a few of the dangers experienced by HIV patients administered AAS for extended periods. Of greatest concern is the increasing numbers of individuals who are currently being treated with AAS to increase muscle mass either for medicinal or recreational means without attention being given to periodically returning the HPGA to normal. With roughly 4 million men in the U.S. being considered hypogonadal (Lacayo R., 2000; Sheffield-Moore et al, 1999; Shelton DL, 2000), an estimated 200,000 men are currently receiving testosterone treatment for the condition (Shelton DL, 2000). As stated earlier, AAS are being prescribed to HIV & AIDS sufferers to combat progressive muscle loss. The Centers for Disease Control and Prevention (CDC) reported an estimated 635,000+ men diagnosed with AIDS through December 2000 while an estimated 97,700 have been reported with HIV (Centers for Disease Control, vol.12, No. 2, table 5; Centers for Disease Control, vol. 12, No. 2, table 6). In 2000 alone over 31,000 men were diagnosed with the AIDS virus (Centers for Disease Control, vol. 12, No. 2, figure 3). Between hypogonadal, AIDS, & HIV males, potentially over 900,000 men are being administered AAS therapy.
Studies recently published on patients suffering from various tissuedepleting conditions and HIV affliction (Bhasin et al, 2000; Grinspoon et al, 1998; 1999; 2000; Rabkin et al, 1999; 2000; Sattler et al, 1999; Strawford et al, 1999;1999; Van Loan et al, 1999) have not identified what should be done to restore normal endocrine status post-treatment. Considering the dosages and compounds administered in many studies, there is no question that subjects were left hypogonadal after therapy. In the cases where the periodic use of testosterone or AAS are necessary, intervention to return the HPGA to normal should be initiated as soon as possible after the cessation of the AAS. As described herein, a possible treatment modality may be the combined regimen of HCG, clomiphene citrate, and tamoxifen. Medical history has demonstrated examples of physician-induced complications resulting from treatment. Iatrogenic hyperthyroidism (Bartsch & Scheiber, 1981) and iatrogenic Cushing’s syndrome (Cihak & Beary, 1977; Kimmerle & Rolla, 1985; Smidt & Johnston, 1975; Tuel et al, 1990) are cases were administered medications or treatments provoked abnormalities in patients’ normal physiology. The administration of testosterone as a treatment for hypogonadotropic hypogonadism falls into this same category of causing endocrine related abnormalities (Bhasin et al, 1996; Marynick et al, 1979; Strawford et al, 1999; Tenover, 1992). Testosterone replacement therapy has proven to be very effective in reversing the symptoms of suppressed testosterone production, but does not treat the underlying cause of the deficiency. Positive effects of testosterone treatment; i.e. improved sex drive, improved sense of well-being, lean body mass; are all transient in light of plummeting gonadotropin levels. Upon cessation of testosterone treatment patients can expect a complete reversal of positive benefits as exogenously influenced testosterone levels metabolize and decline rapidly. Further controlled studies need to be performed showing the combined effects of HCG, clomiphene citrate, and tamoxifen in returning HPGA functioning to normal. Long-term follow-up on these patients returning to normal will be necessary to ensure permanent reversal of hypogonadotropic hypogonadal conditions. In addition, studies documenting dose-response curves for pituitary inhibition and reversal due to AAS administration are critical in determining the correct dose, duration, and form of treatment that is optimal without causing permanent damage. When the need for long-term androgen use presents, using moderately supraphysiologic doses of androgens as suggested by Strawford and colleagues (1999) coupled with post-treatment HPGA restoration as demonstrated here, may be a more effective means over high-dose protocols used to offset negative alterations in lean body mass. Unfortunately current studies have yet to adequately address a standard of patient care post-androgen therapy. Because of the negative impact of the hypogonadal state on physical and mental well- being, pharmacotherapy that restores HPGA function more rapidly than current modalities would greatly benefit men with hypogonadotropic hypogonadism.
While we believe that the treatment protocol was effective in returning normal hormonal function to these men, the lack of randomization or a control group leaves room for speculation. Although cases of spontaneous return to eugonadism with no medicinal intervention have been published, these reports documented durations anywhere from 6-18 months before normal hormone status was achieved (Gazvani et al, 1997; Wu et al, 1996). If the alternative treatment modality described herein can reverse suppressed gonadotropin production and AAS associated side effects much sooner than non-treatment, further evaluation of this therapy should continue.


P

[deleteduser0002]

With good clinical data supporting hcg+NOLVA+clomid.....why do so many recommend aromasin+clomid+hcg?

[gustavo77]

I would have to disagree with that. HCG is definitely needed even if run during the cycle depending on the individual. You cannot generalize things this way at all.
Even if used at a low dose 500iu per day for a couple days on cycle will not be enough for some to recover on clomid alone. Ive seen this first hand on many BB's it just doesnt work. Guys seem to think a dosage over 500iu is going to damage leydig cells etc...this is just not the case. The manufacturer of Canadian Pharmaceutical grade HCG suggests the dosage for hypogonadal men as 4000-5000iu 3-4 times weekly for 6 weeks.
P

I am not talking about using HCG for a few days @500iu than starting clomid, I am talking about using HCG from the very beginning of the cycle to the end...not allowing the leydig cells of the testes to shut down at ALL...at that point PCT is all about restoring pituitary secretion of LH....clomid is all that is needed to do this...and making sure estrogen is kept under control...aromasin being the most effective AI..

[Drummer]

HCG is mainly used in medicine for fertility, and can often be given in doses that will permanently damage a mans testicles. Kinda like the "last hope" effort to conceive. Dont know if I would touch those doses. I dont pretend to know everything about the medical application of HCG, just that the doses can be mega high.

What im interested in is tried and true (even bro science lol) doses that prevent shrinkage during cycle. Especially those long deca or tren cycles. Preatorian was saying the low doses dont do anything....?

~D~

[punkrock]

I think any of these are way better than back in the day where you they just juiced for a long time, took a little break, and jumped back on it. hahaha

Other than that, everything I've read seems to recommend something like aromasin or amiradex.

Aromasin during cycle even. I think next cycle i'm going to use hcg and aromasin during and see if I can bump up the test without side and throw in some tren.

[gustavo77]

With good clinical data supporting hcg+NOLVA+clomid.....why do so many recommend aromasin+clomid+hcg?

I have the link to the study on my other computer but Aromasin has been shown to increase natural test in hypogonadal by 60%....

[kloan]

I am not talking about using HCG for a few days @500iu than starting clomid, I am talking about using HCG from the very beginning of the cycle to the end...not allowing the leydig cells of the testes to shut down at ALL...at that point PCT is all about restoring pituitary secretion of LH....clomid is all that is needed to do this...and making sure estrogen is kept under control...aromasin being the most effective AI..
Isn't that risking becoming desensitized to ones own production of LH?

I personally started running it my 8th week into my cycle with only 250iu 2x week and found it started working within a week... and stopping a few days before PCT.

I wanted to run it throughout my entire cycle, beginning to end, but was concerned of the risk of becoming desensitized to my own LH production.. even at low doses (250iu twice/week).

[gustavo77]

That doesnt mean it isnt the most effective and efficient PCT protocol either.


No it doesn't bro, no it doesn't...there is always gonna be something better out there if we continue to learn.

[Drummer]

...

[Drummer]

I think any of these are way better than back in the day where you they just juiced for a long time, took a little break, and jumped back on it. hahaha

Other than that, everything I've read seems to recommend something like aromasin or amiradex.

Aromasin during cycle even. I think next cycle i'm going to use hcg and aromasin during and see if I can bump up the test without side and throw in some tren.

careful with cutting estrogen while on cycle... you can hinder your gains and maybe hurt the joints.

~D~

[Drummer]

Isn't that risking becoming desensitized to ones own production of LH?

I personally started running it my 8th week into my cycle with only 250iu 2x week and found it started working within a week... and stopping a few days before PCT.

I wanted to run it throughout my entire cycle, beginning to end, but was concerned of the risk of becoming desensitized to my own LH production.. even at low doses (250iu twice/week).

Those doses dont work for me

~D~

[Praetorian]

I am not talking about using HCG for a few days @500iu than starting clomid, I am talking about using HCG from the very beginning of the cycle to the end...not allowing the leydig cells of the testes to shut down at ALL...at that point PCT is all about restoring pituitary secretion of LH....clomid is all that is needed to do this...and making sure estrogen is kept under control...aromasin being the most effective AI..

I understand what you posted..."the entire cycle". That is what i disagree with as I have worked with many BB and run that protocol myself and without HCG at the end recovery did not happen as it should.
HCG used during the cycle still will not help many who are on heavy and long cycles...its just not enough.
P

[waderow]

the prolonged use of HCG scares me more then the high dosed PCT protocols when considering desensitizing

[Praetorian]

HCG is mainly used in medicine for fertility, and can often be given in doses that will permanently damage a mans testicles. Kinda like the "last hope" effort to conceive. Dont know if I would touch those doses. I dont pretend to know everything about the medical application of HCG, just that the doses can be mega high.

What im interested in is tried and true (even bro science lol) doses that prevent shrinkage during cycle. Especially those long deca or tren cycles. Preatorian was saying the low doses dont do anything....?

~D~

That is incorrect...see package insert on Canadian produced HCG...it lists the indications of the drug...fertility is only one of many. recommended doses of HCG ie directly off the package insert from the manufacturer 4000-5000 3-4 times per week does not damage the leydig cells...over exposure can desentitize them to LH.
P

[Praetorian]

the prolonged use of HCG scares me more then the high dosed PCT protocols when considering desensitizing

Bingo!
P

[Drummer]

^^ is this an issue? 4-5000iu 3 times a week = 3 vials a week... for how many weeks? That can get very pricey too...

~D~

[Solo59]

Those doses dont work for me

~D~

I run 500 iu 2x EW. That works, & it's easy to break down a 5000 iu bottle into ten equal injects. This means a 5000 iu bottle lasts five weeks, so it should still have potency on inject #10. (It always seems I'm randier the day after an inject, too, but that could be anything.)

Did not change the HCG protocol off-cycle because I'm now switched back to exogenous testosterone gel & may still need the HCG. My spawning days are over, so I might as well keep the old bones, organs, & muscle feeling & looking hale & hearty as long as possible.

I used to end cycles (in which I used no HCG) with 1000 iu of HCG each day for 10 days straight. Maybe it was in my mind, but during that time I felt I was always on the verge of orgasm.

Solo

[Praetorian]

^^ is this an issue? 4-5000iu 3 times a week = 3 vials a week... for how many weeks? That can get very pricey too...

~D~

Six weeks as quoted on the insert by the manufacturer in Canada. Personally I limit it to 3 weeks.
P

[gustavo77]

the prolonged use of HCG scares me more then the high dosed PCT protocols when considering desensitizing

HCG is prescribed by HRT docs for much longer periods of time than a standard cycle length...

What scares me the most is having the cells of my balls go dormant for 12+ weeks and then having to blast them with high doses of HCG to get them working again...too me that's ****ing scary shit right there...

I am not saying that this dose or that dose will work for everyone cause everyone is different...but there are starting points...for me 500iu of HCG 2x per week keeps things working...my last pct, i ran 1000iu of e3rd day for the last two weeks while the test E was clearing....waited 4 days after my last shot of HCG and then hit the clomid and aromasin....recovery was good..

[gustavo77]

I understand what you posted..."the entire cycle". That is what i disagree with as I have worked with many BB and run that protocol myself and without HCG at the end recovery did not happen as it should.
HCG used during the cycle still will not help many who are on heavy and long cycles...its just not enough.
P

As i said in my above post...everyone is different and some based on their own chemistry and level of cycle suppression will need more HCG near the end...that still does not negate the need to keep the testes working on cycle...recovery becomes more difficult the longer the leydig cells are shut down...

[Drummer]

As i said in my above post...everyone is different and some based on their own chemistry and level of cycle suppression will need more HCG near the end...that still does not negate the need to keep the testes working on cycle...recovery becomes more difficult the longer the leydig cells are shut down...

I would have to agree with that... it takes forever to grow my boys back when then have shrunken to half their size. I havent taken 15000iu a week either... so i have no basis for comparison. I just cant see my boys growing back in 3 weeks with a mega blast of HCG. But again, i havent tried...

~D~

[punkrock]

careful with cutting estrogen while on cycle... you can hinder your gains and maybe hurt the joints.

~D~

Yeah, I only used 12.5mg when I first started getting acne and the nips puffed out a bit. A little estrogen is probably good for a guy, lubes everything up supposedly due to progesterone? right?

[Praetorian]

As i said in my above post...everyone is different and some based on their own chemistry and level of cycle suppression will need more HCG near the end...that still does not negate the need to keep the testes working on cycle...recovery becomes more difficult the longer the leydig cells are shut down...

Just a clarification...i dont disagree with the low dose use during the cycle...i think that is a good idea, just the idea that that may be enough without using hcg at the end...it may be for some ...for other it wont be.
;o)
P

[Drummer]

Yeah, I only used 12.5mg when I first started getting acne and the nips puffed out a bit. A little estrogen is probably good for a guy, lubes everything up supposedly due to progesterone? right?

yes. only cut estro if you have to. As for the rest of the posts, great debate! Ppl will get lots of HCG insight here which is kinda what i was aiming for ;)

~D~

[gustavo77]

Just a clarification...i dont disagree with the low dose use during the cycle...i think that is a good idea, just the idea that that may be enough without using hcg at the end...it may be for some ...for other it wont be.
;o)
P

Sorry for the misunderstanding...i am 100% in agreement with you, that some guys made need more HCG at the end of the cycle....everyone is indeed different.

[GYMBRAT]

Good post bro...very much along the lines of what i recommend...

I do think though that HCG can be used too frequently...shots taken every 3-4 days is optimal. Shot taken any closer together, say ED or EOD can cause over-stimulation and actually damage the leydig cells of the testes. HCG causes peak output of the testes in 48-72hrs.. I have actually read that the testes respond best to this type of "pulse" dosing, every 3-4 days, as it mimics the body's own release of LH. Not sure how accurate that is but every 3-4 day dosing on cycle has worked well for me...even at my age...haha..

I agree with this 100% and seems to be the most effective in my own opinion from my own past experiences. (everyone is different)