I found this on another board. It's written by "Prisoner#22", a respected member who claims to have a medical background. I think it makes sense and a few other senior members of the board agree with him. In the thread he made 6 posts where he explains the why's and how's. I know it's long but I think it's an interesting read.
That being said, here it is:
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absolutely not.
Testicular atrophy is a figment of people's imagination.
Just because testicles appear smaller while on cycle does not mean it has actually shrunk. Instead it is much like the penis or a bicep- when it isn't having sex, it is flacid, when it isn't being worked it is soft, when the body parts are working they become encorged with more blood. Same thing with the testicles.
using HCG just creates another level of suppression in the htpa. It desensitizes the leydig cells to your bodies own LH production, making it so that the hypothalmus and pituitary can be fully recovered and functioning normal, but the testicula axis is still suppressed, due to it's failure to respond sufficiently to your own LH production.
Basically it just makes your ultimate recovery more prolonged.
Best pct is to use a low dose hrt test bridge, gradually reducing the test on a weekly basis untill your own natural production takes over. This will provide the most seamless transition, with the least amount of side effects/ withdrawal symptoms.
tapering is a conventional practice widely used in medicine
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O.k and what kind of qualifications do you have??? I'm a medical proffessional, and I can tell you that there is no such studies out there that prove there is a need for hcg use in order to recover full function of the hpta in a eugonadic male. In fact, why would you add a drug into the mix that actually causes suppression at another level of the hpta? It's just ludecrous, the reasoning behind it is much like hitting your head with a hammer to distract you from your sore thumb.
I am a medical proffesional and I will tell you that there are too many 'know-it-all's' on these boards who go around rehashing someone else's posts to increase their 'reputation' when they actually do not know what the hell they are talking about, have no understanding of physiology, and pharmacology, and absolutely no skills at been able to critique research in the first place.
On top of this there are so many BB out there who don't understand the concept of a 'half-life' , that they start their pct way too early, and when nothing happens, and their balls are still small (due to the fact their actually still 'on') they shoot themselves up with HCG which causes their balls to swell, and their libido to pick back up, and they think they have recovered. Of course, unbeknownst to them, the effect is just temporary, sooner or later after they stop the hcg their libido lags and their test drops back down again. But by that time they are in denial of the fact, not wanting to admit to anyone that their pct has failed, and they end up jumping back on a cycle lickity split, to fix the problem.
This happens all the time.
Hcg use is just plain harmfull in a eugonadic male. I wouldn't recomend it's use to anyone on a steroid cycle.
When the body is trying to come back to homeostasis, why would you throw all that extra junk of hcg and serms into the mix?
The truth is a simple hrt taper - gradually reducing the dose of exogenous testosterone, as endogenous testosterone levels increase, is not only the most seamless pct, but also offers the least side effects, and withdrawal symptoms. Tapering is also considered standard practice for cessation of all receptor mediated drug therapies in medicine.
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Well to back track on what I have said: the use of hcg is primarily in veteranarian applications, for causing ovulation,and increases in sperm counts to ensure propagation of the heard. They don't care about the animal's libido. It is the same in humans, it is primarily for giving the best chance at pregnancy, not for use in post cycle recovery of steroids. Yes of course if you have a pituatary insufficiency of LH secretion, then there are definite reasons for using hcg for hrt purposes.
The problem is that as men age, Lh production normally does not fall off, it is actually the testicles ability to respond to the LH that wains.
Now everyone has heard the 'theory' that hcg causes desensitization of the leydig cells to your own natural hormone. Well this is true. In the end, of course eventually the body will readjust, however temporarily, you become just as dependant on hcg, as you were on steriods, and I am talking of using as little as 250-100 iu at a time. How do I know this? from experience of course, as I was once 'fooled' by Swale's approach but I have tried it both ways and the verdict is in: recovery is much easier without hcg then with.
So why the hell would you even think of using hcg in the first place? Why would you unnessessarily cause suppression on a whole different level, within your axis?
The reason why is that someone fooled us all into thinking that testicular atrophy actually occurs??? and that it is a real concern, that it will hinder recovery. Well the truth is that is a pack of lies. Yes while on cycle the testicles may 'feel' smaller, however, it is just because of lack of blood flow to the area. Same principle as any other body part - when it is working hard it becomes engorged with extra blood. When it isn't it is not engorged with blood and feels smaller, and cooler. That of course doesn't justify the need to pump hcg into your body, if it bothers you, just use a little bit of mueler's hotstuff to the area, and I guarentee it will become warmer and more swollen, and with out the added suppression .
So if hcg isn't the answer what is? Well the bottom line is this... Keep things simple. Don't flood your body with a whole lot of crap like serms and hcg and other things that are just going to complicate the processes of reachieving homeostasis post cycle.
All you need is an AI to ensure that estrogen levels do not rise above normal levels. And for those who think you need high levels of estrogen to 'maximize gains' that is a myth, all you are actually doing is retaining more water and fat, and killing testicuar cells in the process.
So basically continue the AI all the way through the cycle and taper it as the testosterone tapers out of your system, to ensure there is no 'rebound' effect at cycle's end.
The key however is that synthetic testosterone must be the last compound to leave your body, or recovery will be much harder and longer. Compounds like nandrolone or trenbolone that convert to progesteone, do not convert to dht, and bind well to the AR should always be the first coupounds to leave your system. Testosterone -which is indistiquishable to your own hormones by your body should be the last, as I have said.
Now I'll thank bulk muscle for some of his research in this area as he came up with this study:
http://ajpendo.physiology.org/...ull/281/6/E1172
that refutes the point that some experts might argue, that if there is any exogenous testosterone in the body, then the endogenous production of test is completely suppressed. This is their argument to why tapering does not work, however, according to the study in order to achieve their results they had to use an LH antagonist, so they could get accurate measurements, of the subjects taking the different weekly doses of testosterone. So this shows that as long as blood testosterone levels are lower than the body's natural needs, the hpta will not be suppressed, and will produce testosterone to pick up the slack.
So to recapp:
exogenously injected testosterone is indistinguishable to the body from it's own, as it is the exact same molecule.
As levels of exogenous testosterone fall below what the body normally needs, the body will via the negative feed-back loop - sence this, and begin producing testosterone to pick up the slack.
As exogenous levels fall further, endogenous levels will continue to rise to a point where exogenous levels fall off altogether, and the hpta takes over as the only source for testoterone again.
Since the tapering process is slow, the body has plenty of time to get the testes in good working order, so no need for the hcg use that dominates the rationale for administering hcg in the first place.
Its simple and it works.
The key is ensuring that all other steroids have long left the body before begining the hrt taper, to ensure there isn't any non-dht converting steroids to mess with libido, or progesterone converting steroids e.t.c Basically, in order to be successfull you need to clean out of all non-testosterone steroids from your body, before you can begin the hrt taper.
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Well as I have stated, alway use an A.I. with the test to ensure estrogen levels do not escalate out of control. This is by far the most important part of the taper!!!.
Estrogen hangs around in the body for a long time. If these levels are too, high, your taper won't work, as the hpta will still be shut down due to these high levels.
I recomend .5 mg of arimidex daily throughout the 500mg of test per week cycle. At the end of the cycle, it will take roughly 4 weeks for levels of exogenous testosterone to fall off. During this time, continue to do .5mg of arimidex daily for two weeks, then reduce the dose to .5mg of arimidex every other day for 1 week, and then .25mg of arimidex eod for 1 week.
As testosterone enanthate tapers itself, and the body can't distinguish exogenous test from endogenous, there shouldn't be any need for using hrt test during this period.
At the end of this 4 week period continue with the arimidex at .25mg eod for 2 additional weeks, to ensure estrogen aromatization continues to remain low, and that there is no 'rebound' effect when you go off the arimidex, as can happen if you stop it too soon.
That is all that should be needed for a straight testosterone cycle - the key as I said is keeping estrogen in check from the get-go! nolvadex and clomid will not suffice for this! you absolutely have to use an AI!!!!
Now, at this point if you wanted to try a SERM that would be the point to begin it's use.
Now suppose you were on a cycle of say Nandrolone decanoate at 600 mg per week. What would you do for pct using the testosterone taper approach?
Well this is how you would approach it. If you were taking any aromatizable products beside the nandrolone, ensure that you use an aromatase inhibitor from the start.
After your last injection of Deca, you have approx. 6 weeks before your body is even ready to begin recovery. Nandrolone doesn't convert to dht, and converts to progesterone, and binds strongly to the AR, so not only is it suppressive via progesterone, and the strong binding affinity, as it tapers, your body will only be able to produce a small amount of testosterone that converts to dht, and since deca, does not, the overall amount of dht (for supporting a libido) will be insufficient, hense the 'deca dick' syndome.
For this reason, you need to add dht into the mix for that 6 week period, while the deca tapers. The easiest way is to use testosterone enanthate at 100mg per week for this six week period. Remember to continue the AI thoughout!
You can however also use proviron at 50 mg per day, or masteron (I prefer enanthate) at 100mg per week. or a combination of test and masteron which works well also. (I will address this futher).
Now at the end of the six week stage, start using testosterone at 100mg per week for two weeks. this will ensure the deca is not going to complicate things. At this point reduce the dose to 75 mg per week. Wait two weeks. If the libido is unchanged, then further reduce the dose to 50 mg per week. Your decision to reduce the dose is completely subjective at this point. The indications I got that the pct was working, was an increase in testicular size, and soreness in the area.
I must also note at this amount of test per week you can consider yourself 'off cycle' as all the 'on' cycle symptoms will have dissappeared - i.e crazy pumps, e.t.c. Your body will be normalizeing itself - by this I mean if you stayed on this dose, and then in 6 weeks hit another cycle, your body would respond to the steroids as if you had not been on anything, and good new gains could be achieved - not just gaining back lost size.
There is no need in my opinion to further reduce the dose from 50 mg per week. You can go off at this point, and expect a full recovery. Just contine the arimidex, for an additional two weeks at .25mg eod, to ensure no estrogen rebound.
after that, as I said earlier would be the time to use a SERM like nolva or clomid if you wished.
so the protocol should look something like this:
6 weeks after your last injection: 100mg Test E/ week, .5 arimidex eod.
7 and 8 weeks post final inject: 100 mg Test E/ week, .25 mg arimidex eod.
9 and 10 weeks post final inject: 75 mg Test E/ Week, .25mg arimidex eod.
11 and 12 weeks post final inject: 50 mg Test E/ Week, .25mg arimidex eod.
13 and 14 weeks post final inject: No injections .25 mg arimidex every third day.
Week 15 on: option to try a SERM or nothing at all, or go back on cycle
Now as I said before, you can use masteron with test, and instead of arimidex. Masteron was origionally a breast cancer drug (hense the word 'mast' as in mastectomy), and was used for it's anti-E properties, and it also is DHT, so it will maintain libido as well, and bind more advidly to SHBG, then the hrt test E, and your own natural test.
I would also highly recomend it btw for those using hrt on a long-term basis, who suffer from gynocomastia sides, as it would alleviate this problem, yet allow them to get the effect from the testosterone that they desire.
I have used it in a 50/50 split with test E, during the hrt taper with good success. - just start off with 50,g of test E/ week and 50 mg of masteron E per week and taper according to the above protocol, always keeping a 50/50 ratio.
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Nolvadex and clomid are molecules shaped like estrogen which compete with estrogen at the estrogen receptor site. They themselves can only exert weak estronic effects, therefore, they prevent gynocomastia, and can fool the hpta into secreting LH, which causes the testicular axis to increase testosterone production. The drugs do not prevent testosterone from converting to estrogen, which can lead to very high estrogen levels that don't magically go away. When nolva and clomid therapy are stopped, the possibility of an estrogen rebound is very likely. This causes, shutdown of the hypothalmus-pituitary-testicular-axis (hpta), which inturn leads to low test levels, fat retention, water retention, muscle loss, no libido, and depression. As well as I have stated before high levels of estrogen are linked to testicular cell death, and prostate cancer, never mind late onset gynocomastia.
Instead Arimidex (anastrozole), and Femara (letrozole) are aromatase inhibitors. Testosterone is only converted to estrogen because an enzyme called aromatase binds to the testosterone molecule, and catalyzes the conversion to estrogen. Arimidex and femara are aptly called aromatase inhibitors, because that is what they do. They inhibit the aromatase enzyme from binding, therefore no conversion can take place.
By using an AI you can keep your estrogen levels at normal masculine physiological levels throughout the cycle, and through pct, and not have to worry about a 'rebound' post cycle. This is called eating your cake and having it too .
As for retention of muscle, It is the best method. The taper is seemless - there is no test crash. Training does not have to change from on - cycle to of cycle, as there should be no real catabolic stage. Of course you will loose some gains. this is inevitable, as if you are above your natural peak, there is no way your body will be able to support all of your gains. This is just the reality of it.
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Not using an AI certainly doesn't put an axe in the method, however as I stated earlier, There are definite health risks to having elevated blood estrogen in a male, and it will complicate your pct.
Many don't realise how long it takes for estrogen levels to drop. They use nolva or clomid, during and after their cycle, and then once they go off their libido drops, and they begin to develpe late-onset gynocomastia - puffy nipples e.t.c, of course along with loss of gains, fat and water retention, and a testosterone crash. This is because estrogen levels are still high, but the estrogenic effects are being kept at bay by the receptor antagonists (nolva, clomid). Once these are stopped, estrogen is free to bind again, and that is what causes the rebound effect.
What this means to tapering is that you will have to stay on an hrt dose for a longer period of time, while blood levels of E normalize.
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Originally Posted by c eastwood
