Perfect PCT

[OMEGA]

For novices I wanted to share a really good and
AGGRESSIVE PCT
(some will say its over kill but screw em')
This PCT in for Long acting Esters like a Test only cycle.

I am not going to post more than this solitary post ( unless its for help), for I do not want to argue about nuances or PCT theory......trust what has been written and it will treat you well

A)
5-7 days After Last shot of Test E or Cyp
Start HCG with NolvaDex and Arimadex (or AIFM)

Take 2000 ius of HCG Every 4th day for a total of 4 shots ( thats 16 days of being on HCG)
During this time because your coming Estrogen will be HIGH
Estrogen to T levels will start to veer toward Estro.
Take 30 mgs of Nolva, and 1 mg of Arimadex to start suppressing it and to close the feedback loop to kick start Test levels again.

B)
After the last shot of HCG Start Clomid Therapy along with conventional PCT
(no front load of clomid)
also take it with Nolvadex and Arimadex (or AIFM)

take Clomid like this:
10 days 100 mg a day
10 days 75 mg a day
10 days 50 mg a day

take Nolvadex like this:
10 days 30 mg a day
10 days 20 mg a day
10 days 20 mg a day

Arimadex

1 mg a day for 30 days ( or AIFM)

 

[bw1]

I have seen pct similar to this, but with Aromasin instead of Arimidex. Looks good

 

[Mr.X]

For

take Arimadex like this:
10 days 30 mg a day
10 days 20 mg a day
10 days 20 mg a day

Arimadex

1 mg a day for 30 days ( or AIFM)

I'm assuming you mean Arimidex, 30mgs per day?? did you mean nolvadex?

 

[guitrole1]

For novices I wanted to share a really good and AGRESSIVE PCT
(some will say its over kill but screw em')
This PCT in for Long acting Esters like a Test only cycle.

I am not going to post more than this solitary post, cus I dont want to argue about nuances or PCT theory......trust what I wrote and it will treat you well


I fit into this category and I have a been reading everything I can about PCT. I'm not trying to argue about the nuances of PCT theory, but I do have a couple questions for you. First, what if there is no HCG available? Is it crucial to a quality PCT? Second, do you recommend taking anthing during the cycle or just react to any negative sides such as gyno on an individual basis?

Thanks, just trying to learn.

 

[Mr.X]

what if there is no HCG available? Is it crucial to a quality PCT? .

HCG is not crucial for PCT in most cases, unless you're on a long tren cycle.

 

[OMEGA]

First, what if there is no HCG available? Is it crucial to a quality PCT? .

after a long cycle it is most helpfull, I would say "crucial"

 

[guitrole1]

after a long cycle it is most helpfull, I would say "crucial"

So, would you consider a 10wk 500mg/wk test-e only cycle fitting into this category?

 

[OMEGA]

its on the line,
HCG def cant hurt

 

[swordfish151]

HCG is not crucial for PCT in most cases, unless you're on a long tren cycle.

Define "long tren cycle" ... more then 6 weeks?

 

[OMEGA]

yep

 

[Sanel27]

Good post bro, im kinda novice still (only 3 cycles under my belt) but i dont have access to Arimidex as my source doesnt sell it (very costly) but i do have Nolvadex and Clomid.

Never tried HCG but i will give it a try this time around as im planning to do Deca/Test/Var in the upcoming cycle. Never tried Deca but heard that it shuts you down hard so ill get HCG and hope that helps.

Thanx for posting the dosages as that will come in handy

 

[The Iotola]

take Clomid like this:
10 days 100 mg a day
10 days 75 mg a day
10 days 50 mg a day

take Nolvadex like this:
10 days 30 mg a day
10 days 20 mg a day
10 days 20 mg a day

Arimadex

1 mg a day for 30 days ( or AIFM)[/QUOTE]

If one did a light cycle of 400mg/Test would 30 days be too much? Would 21 be sufficient?

 

[Zuperman]

Should this be made a STICKY????? I THINK SO.....SO THE NEWBIES DONT HAVE A HARD TIME LOOKING FOR IT, AND START ASKING Q'S?
K 2 U BRO!!

 

[Mr.X]

Define "long tren cycle" ... more then 6 weeks?

Over 8-10 weeks is long IMO. I've recovered without HCG after 6 weeks, no problem.

 

[OMEGA]

take Clomid like this:
10 days 100 mg a day
10 days 75 mg a day
10 days 50 mg a day

take Nolvadex like this:
10 days 30 mg a day
10 days 20 mg a day
10 days 20 mg a day

Arimadex

1 mg a day for 30 days ( or AIFM)

If one did a light cycle of 400mg/Test would 30 days be too much? Would 21 be sufficient?[/QUOTE]


do it for 30, it cant hurt

PCT is the time where it pays to be a bit over the top ( within reason)

 

[OMEGA]

Good post bro, im kinda novice still (only 3 cycles under my belt) but i dont have access to Arimidex as my source doesnt sell it (very costly) but i do have Nolvadex and Clomid.

Never tried HCG but i will give it a try this time around as im planning to do Deca/Test/Var in the upcoming cycle. Never tried Deca but heard that it shuts you down hard so ill get HCG and hope that helps.

Thanx for posting the dosages as that will come in handy

drop the deca a good 4-5 weeks before your last shot of Test, Deca has the nasty habit of lingering.......

 

[Mammoth2500]

Over 8-10 weeks is long IMO. I've recovered without HCG after 6 weeks, no problem.

What were you on for your 6 week cycle?

I have recovered fine with no HCG with an 11 week cycle with just tribulus and nolva.

 

[Slyder190]

I'm a beleiver of an agressive PCT. We oput together "killer" cycles, why not a "killer" PCT? I am in favor of HCG no matter what. Since I've used in recnet times, I personally haven't had any of the crash effects I had become acustomed to.

 

[c gheller]

Im startin PCT in two days. I like the look of this, so im going to give it a go.

 

[OMEGA]

Im startin PCT in two days. I like the look of this, so im going to give it a go.

good luck

remember with all that coverage the possible TEMPORARY side effects may be tender joints ( esp with adex) and mood issues

but 1 month of sacrifice is worth Months of Gains, not to mention adequate HPTA recovery.

 

[Alpine`]

For novices I wanted to share a really good and
AGGRESSIVE PCT
(some will say its over kill but screw em')
This PCT in for Long acting Esters like a Test only cycle.

I am not going to post more than this solitary post ( unless its for help), for I do not want to argue about nuances or PCT theory......trust what has been written and it will treat you well

A)
5-7 days After Last shot of Test E or Cyp
Start HCG with NolvaDex and Arimadex (or AIFM)

Take 2000 ius of HCG Every 4th day for a total of 4 shots ( thats 16 days of being on HCG)
During this time because your coming Estrogen will be HIGH
Estrogen to T levels will start to veer toward Estro.
Take 30 mgs of Nolva, and 1 mg of Arimadex to start suppressing it and to close the feedback loop to kick start Test levels again.

B)
After the last shot of HCG Start Clomid Therapy along with conventional PCT
(no front load of clomid)
also take it with Nolvadex and Arimadex (or AIFM)

take Clomid like this:
10 days 100 mg a day
10 days 75 mg a day
10 days 50 mg a day

take Nolvadex like this:
10 days 30 mg a day
10 days 20 mg a day
10 days 20 mg a day

Arimadex

1 mg a day for 30 days ( or AIFM)

The core of any PCT should be a serm such as Nolvadex. If its a long/harsh cycle the use of HCG may also be desired. An AI alone (such as ATD) is a very unwise choice for PCT. A lot of recovery/PCT ATD products are being sold right now.

I really dont feel that an AI is needed at all but some do. There are arguments on both sides.

Here is a good PCT write-up incorporating Nolva/HCG and aromasin. Scroll down toward the bottom for the weekly layout.

http://www.avantlabs.com/magmain.php?pageID=431&issueID=35

 

[dr_skier]

Ok please no flaming.

If one were to encorporate a 3week 10mg dbol bridge while on pct to maintian gains and keep the sex drive up, would one do 10mg am through the two weeks off (while on hcg) through the clomid and say stop with one week of clomid and nolva left? OR perhaps extend it a week so you are doing a bridge for say 21 days followed by more clomid and novla for 2 weeks?

I'd love to hear omega or mr. X's comments on this. If the comments are in fact not to do it can you guys perhaps just list some pros and cons. Thank you.

 

[Alpine`]

Ok please no flaming.

If one were to encorporate a 3week 10mg dbol bridge while on pct to maintian gains and keep the sex drive up, would one do 10mg am through the two weeks off (while on hcg) through the clomid and say stop with one week of clomid and nolva left? OR perhaps extend it a week so you are doing a bridge for say 21 days followed by more clomid and novla for 2 weeks?

I'd love to hear omega or mr. X's comments on this. If the comments are in fact not to do it can you guys perhaps just list some pros and cons. Thank you.

First of all - DBOL, Bridge, and Recovery dont mesh well together. If you are on any AAS (even a low dose) you are not in post cycle recovery. Technically you are still on your cycle. Your natural testosterone is supressed and the "recovery" process cant fully begin. A bridge is nothing more than an extension of the cycle and should be considered as such. You cant have your cake and eat it too. Either you are on or you are off. A proper PCT and recovery cant take place until you are off AAS. I know it sucks but thats the way it is.

 

[c gheller]

Omega...So this is a 46 day total PCT right? 16 days HCG and Nolva, then 30 days Clomid and Nolva?

 

[OMEGA]

Omega...So this is a 46 day total PCT right? 16 days HCG and Nolva, then 30 days Clomid and Nolva?

30 days conventional PCT remember Test take about 14-20 days to clear in a fashion that allows for recovery with conventionl PCT

HCG is used just before to kick start things again for certain

 

[dr_skier]

fair enough omega, sigh, cake..... i like cake.

However, best post i've ever read on pct, straight-foreward, pct for dummies guide if u will, kudos.

Actually, here's a pct question then. Jentic's pct advises the use of hcg in increments of 1500iu eod while on nolvadex. Any comment in the pct comparison?

 

[OMEGA]

my comments are done on this thread
for some PCT is like Religion to each his own.......

-FIN-

 

[macrophage69alpha]

The core of any PCT should be a serm such as Nolvadex. If its a long/harsh cycle the use of HCG may also be desired. An AI alone (such as ATD) is a very unwise choice for PCT. A lot of recovery/PCT ATD products are being sold right now.

I really dont feel that an AI is needed at all but some do. There are arguments on both sides.

if this had been posted in another thread, there would not have been any issue. Its a valid argument that AI's alone may not be the best option for PCT. However if you are going to reccomend HCG or LUTROPIN, particularly HCG then an aromatase inhibitor is essential.

IMHO PCT is best comprised of low dose HCG or lutropin, a SERM, A dopaminergic (low dose) preferably something like selegiline (mao-i-b) and an AI.

there is still widespread debate on which serm, which AI, which dopaminergic are best.

 

[krishna]

What do you guys at AF think of tribulus? I know the studies are limited, but doesn't this herb stimulate LH. If someone didn't have HCG, would trib be the next best thing?

 

[macrophage69alpha]

What do you guys at AF think of tribulus? I know the studies are limited, but doesn't this herb stimulate LH. If someone didn't have HCG, would trib be the next best thing?

unfortunately there is absolutely no evidence that tribulus works. All of the non biased research shows quite the opposite.

Early batches, that did have effect (they worked.. really), were likely "spiked" with SERM's.

its like hot stuff, every body loved it, swore by it, when it was spiked with dianabol

 

[Alpine`]

if this had been posted in another thread, there would not have been any issue. Its a valid argument that AI's alone may not be the best option for PCT. However if you are going to reccomend HCG or LUTROPIN, particularly HCG then an aromatase inhibitor is essential.

IMHO PCT is best comprised of low dose HCG or lutropin, a SERM, A dopaminergic (low dose) preferably something like selegiline (mao-i-b) and an AI.

there is still widespread debate on which serm, which AI, which dopaminergic are best.

What you say on the open forums and what you actually do are two different things. I said ATD for PCT was a bad call and my post was promptly deleted and my account suddenly expired. You did a little damage control later but thats beside the point. I lost a great deal of respect for EF today. If it werent for a few good mods I wouldnt even be here anymore. Im done with this subject. There is nothing more to sweep under the rug. I'll probably end up banned again. Im done speaking against any of AF's products. I'd rather be able to at least browse the forums.


btw, Swale commented on the subject. AI's have no place in PCT according to him. I agree with you on one aspect, with HCG it might be wise. Im far less educated than you or he on the matter though.

-----------------------------------------

.. dont post links to the same slander... if you wish to repost swales opinions on the matter that is fine....

 

[macrophage69alpha]

What you say on the open forums and what you actually do are two different things. I said ATD for PCT was a bad call and my post was promptly deleted and my account suddenly expired. You did a little damage control later but thats beside the point. I lost a great deal of respect for EF today. If it werent for a few good mods I wouldnt even be here anymore. Im done with this subject. There is nothing more to sweep under the rug. I'll probably end up banned again. Im done speaking against any of AF's products. I'd rather be able to at least browse the forums.

you are a child. Whose perceptions and memory are erroneous.

your post was edited because you cant discern the difference between personal attacks and science or even couretous dialogue for that matter. The argument which you made here again was left untouched merely the libel and character attacks were removed. You were suspended for 3 days because after being warned you continued, not only that but you went back and changed a post that had been edited. That is a violation of the TOS.

if you have any valid criticism, as you did in your post above, you are welcome to make it. But this is not C&C and your baseless personal attacks and slander wont be tolerated.

 

[x_muscle]

Ok lets have a scietific discustion


Posted by Swale

" First, I am a DO, not an MD. More importantly, I am very much up-to-date with respect to current AI's. What I currently prescribe for my patients is Arimidex.

The reason AI's should not be used during PCT is the simple fact you are trying to restore natural balance to the endocrine pathways. Administering a powerful endocrine disrupter in counterproductive to that end. THEN add in the estrogen rebound of AI's, and subsquent increased risk of gyno.

Next, you extend the period the Lipid Profile is trashed, and therefore time of plaque deposition within the cardiovascular system, should you drive E too low--and that is easy to do once the cycle has ended. And no, Aromisin has not been shown to comparatively avoid this risk in male subjects.

Which brings me to another point: scientific studies are grossly misused on these Boards. You simply cannot extrapolate conclusions regarding adult males based upon studies conducted on females. Our bodies are that different.

AI's are to be used during the cycle, to maintain physiological levels of estrogen, and D/C'd once T levels drop to a concentration roughly equal to that induced by 200mg per week IM.

I just don't think anyone who understands how the endocrine system functions would ever recommend an AI for PCT."


----------------

AI alone is not a good idea because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile. Plus estrogen is shown to have some role in recovery.
------------------------

Another reason not to use Ai during PCT. It appears that esrogen has a role in recovery. " Normal hypothalamic level, estrogen may in fact arouse the HPTA. This data may be steady with some information that propose tamoxifen is estrogenic and not anti-estrogenic at this level. This data does not propose any diverse method, describes how it could be probable that nolvadex may be better than Clomid, since it work as an estrogen at the hypothalamus and as an anti-estrogen at the pituitary"
AI decrease estrogen levels to unhealthy levels


Evidence for direct estrogen regulation of the human gonadotropin-releasing hormone gene.

Radovick S, Ticknor CM, Nakayama Y, Notides AC, Rahman A, Weintraub BD, Cutler GB Jr, Wondisford FE.

Division of Pediatric, University Hospitals of Cleveland, Ohio.

This study is an attempt to determine whether estrogen could directly regulate human gonadotropin-releasing hormone (GnRH) gene expression. Human GnRH expression vectors were constructed by fusing various 5' flanking regions of the human GnRH gene upstream of the luciferase reporter gene (LUC) or the thymidine kinase promoter linked to the chloramphenicol acetyltransferase reporter gene (CAT). These constructs were transiently transfected into a human choriocarcinoma cell line (JEG-3) and LUC or CAT activity was measured after either no treatment or treatment with various concentrations of estradiol. A stimulatory estrogen response element (ERE) was localized to a 32-bp region between -547 and -516 bp. To determine whether estrogen receptor bound to this region of the gene, we performed DNase I footprinting using purified calf uterine estrogen receptor. DNase I footprinting demonstrates a strong footprint between -567 and -514 bp of the human GnRH gene. In addition, an avidin-biotin complex DNA-binding assay demonstrated that a biotinylated DNA fragment containing -541 to -517 bp of the human GnRH gene bound 35S-labeled estrogen receptor as well as a biotinylated DNA fragment containing the xenopus vitellogenin ERE. On the other hand, the negative control biotinylated DNA fragment derived from adenovirus 5 bound insignificant amounts of 35S-labeled estrogen receptor. Both the GnRH ERE and vitellogenin ERE bound 35S-labeled estrogen receptor with high affinity (approximately 1 nM). These data indicate that the human GnRH gene contains an ERE sufficient to mediate a stimulatory response to estrogen in heterologous cells. Based upon these data we hypothesize that the human GnRH gene might also be directly regulated by estrogen in the hypothalamus, and that this regulation may explain the GnRH hypersecretion observed at the time of the preovulatory luteinizing hormone (LH) surge.

 

[x_muscle]

Foidart A, Harada N, Balthazart J.

Laboratory of Biochemistry, University of Liege, Belgium.

Castrated quail were treated with Silastic implants filled with testosterone (T) in association with injections of the aromatase inhibitors, R76713 (racemic vorozole; 1 mg/kg twice a day) or 4-hydroxyandrostenedione (OHA; 5 mg/bird twice a day). Control birds received no treatment (CX group) or were implanted with T capsules only (CX + T group). Both R76713 and OHA strongly inhibited the T-activated male copulatory behavior. This inhibition had the same magnitude in both groups. The growth of the cloacal gland, a strictly androgen-dependent process was not affected by these compounds. The treatments significantly affected the number of aromatase-immunoreactive (ARO-ir) cells in each of the six brain areas that were studied: the anterior and posterior parts of the sexually dimorphic medial preoptic nucleus (POM), the septal region, the bed nucleus of the stria terminalis (BNST) and the anterior and posterior parts of the tuber. This number was significantly increased in all areas by T. In agreement with our previous study, R76713 significantly inhibited this effect of T in the tuberal hypothalamus but not in the anterior POM nor in the BNST. By contrast the effect of T on the number of ARO-ir cells was completely blocked by OHA in all brain nuclei. The two inhibitors had statistically different effects in all brain regions. Like in a previous study, R76713 increased the intensity of the staining of all ARO-ir cells. This effect took several days to develop suggesting a progressive build-up of the enzyme concentration. This was also suggested by the fact that a rebound in aromatase activity was observed 16 to 24 h after a single injection of R76713. The increased immunoreactivity was not observed in OHA-treated birds. The denser immunoreactivity in R76713-treated birds and the better tissue preservation due to the aldehyde fixative that had been used provided here a clearer picture of the cellular and subcellular localization of ARO-ir material. This allowed to identify new groups of immunoreactive cells, namely in the nucleus accumbens, in the area of the paleostriatum ventrale, in the nucleus taeniae, in the medial and caudal hypothalamus and in the medial part of the mesencephalon and of the pons. Most of the immunoreactive material was located in perikarya but some of these cells were also surrounded by dense networks of ARO-ir fibers often associated with immunopositive punctate structures.(ABSTRACT TRUNCATED AT 400 WORDS)

1: J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60. Related Articles, Links


Use of ultrasensitive recombinant cell bioassay to measure estrogen levels in women with breast cancer receiving the aromatase inhibitor, letrozole.

Klein KO, Demers LM, Santner SJ, Baron J, Cutler GB Jr, Santen RJ.

Children's Hospital of Orange County, California 92668, USA.

The development of well tolerated, potent, specific, and nontoxic aromatase inhibitors for the treatment of postmenopausal women with estrogen-dependent breast cancer has been a major goal of recent studies. The third generation inhibitors now under investigation are nearly 10,000-fold more potent than first generation compounds. Currently available RIAs for plasma estradiol lack sufficient sensitivity to measure levels during aromatase inhibition and, thus, to assess drug potency precisely. The availability of an ultrasensitive bioassay for estradiol provided the opportunity to accurately assess the potency of a new third generation triazole aromatase inhibitor, letrozole (CGS 20267). We used this assay to measure estradiol levels in 14 women with metastatic breast cancer given letrozole at doses of 100 micrograms to 5.0 mg/day over a 12-week period. The lack of differences between doses and sampling times allowed pooling of data. Basal estradiol levels of 7.2 +/- 1.9 pmol/L (mean +/- SEM, 1.95 +/- 0.52 pg/mL) fell to 0.26 +/- 0.11 pmol/L (0.07 +/- 0.03 pg/mL) during the first 6 weeks of therapy and to 0.48 +/- 0.18 pmol/L (0.13 +/- 0.05 pg/mL) during the second 6 weeks of therapy. Although plasma estradiol levels measured by RIA were significantly correlated with levels measured by bioassay (r = 0.79; P < 0.01), the degree of suppression assessed by the bioassay (95 +/- 2% after 6 weeks) was greater than that determined by the RIA (81 +/- 4%), presumably due to improved ability to measure very low estradiol levels. We conclude that plasma estradiol is suppressed by letrozole to lower levels than previously observed, with equivalent suppression at all doses studied. A slight, although not statistically significant, rebound in estradiol levels occurs during the second 6 weeks of therapy compared to the first 6 weeks. Maximum inhibition of aromatase is achieved at letrozole doses as low as 100 micrograms.

Publication Types:
Clinical Trial

 

[macrophage69alpha]

study #1- all this says is that oestrogen may mediate GnRH, it does not say how. Its pretty clear that all steroid hormones impact GnRH.

Study #2- its clear that oestrogen is necessary, to some extent, for human male desire. Though inhibition of that desire is typically only seen with very heavy oestrogen suppression. (men are not quails)

Study #3- this is old, though relevant, news- aromatase inhibitors are more effective than the early assays indicated. These numbers are reflected in all the post 1995 literature and studies.