Thoughts on Planning PCT

Pharma / TRT
1

In reading through posts here recently, a couple things keep popping up at me, and i hope this will be worthwhile to others in planning PCT…

-Clomid has been shown clinically to decrease in the LH response to LHRH, whereas none of the other SERMs have. this means, that one would prefer another SERM over clomid, unless they are not available, or you’ve experienced an adverse reaction to them. (EDIT-further reading on this shows that this is an issue with megadoses of clomid, and not a normal dose of 25 mg).

-Nolvadex would be generally the preferred choice, unless cancer risk is an issue (then Toremifiene is much better, and it also helps for high prolactin) or clearance for a drug test (then raloxofen would be better, as it clears at least 5x faster). Toremifene has been shown to increase LH and testosterone levels steadily with 3 months of use, whereas Nolvadez for 2 months and Raloxifen seems to only work for about a month… Tamoxifen and toremifen have also shown to lower LDL levels, but Tore might raise HDL (the good cholesterol). however, tore seems to increase SHBG, whereas tamox does not.

-Nolvadex at 20 mg/day has been shown to be as effective as Clomid at 150 mg/day in raising test and LH…

-the practice of combining clomid and nolvadex for PCT, seems to be pointless, at best (and might be slightly counterproductive, and a waste of money). and we know that all AAS exert suppression pretty quick into a cycle, so to presume a couple weeks of a SERM after a 20 week cycle will get the body producing normal hormone levels again is wildly optimistic.

My conclusion: i think it simply might be a better idea for most people to run something like tamox or tore for equal time as the length of the cycle afterwards, up to 3 months… i think that time matters here more than the dosage of the compound in PCT…

A couple references, below:

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basic guidelines, based off this^

-for a basic 8 week test cycle, tamoxifen at 20 mg/day for 8 weeks following the cycle
-for a cycle 12 weeks or longer, tamoxifen at 20 mg/day for 12 weeks following the cycle
-for a cycle that includes tren or deca, toremifene at 60 mg/day for equal time following the cycle (up to 12 weeks)
-for people with a concern about cancer (family history, etc), toremifene at 60 mg/day for equal time following the cycle (up to 12 weeks)
-for an athlete with a drug test coming up, tamoxifen at 20 mg/day for 1 week, followed by raloxifene at 60 mg/day for 4 weeks following the cycle, with at least a week “off” prior to competition. could be taken consecutively or concurrently (stacked).
-for an athlete with pre-existing gyno, raloxifene has a stronger effect on the ER in breast tissue (at 60 mg/day). however, it has a minimal effect on raising LH/test after 30 days…

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also, it should be noted that Arimdex (Anastrozole) and Femara (Letrozole) have their blood levels reduced by tamoxifen. so, Aromasin (Exemestane) should be the preferred choice in PCT when adding in an AI.

Aromasin will assist in PCT, as low estrogen levels will convince the HPTA to increase testosterone levels… which makes sense, as Aromasin has been shown to raise testosterone levels by itself.

EDIT: when combining Aromasin and a SERM, one should prolly stop one or the other a week later… if not, the ER would be active again (from the cessation of the SERM) and estrogen levels would be coming back up to normal (with the cessation of the AI).

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I’ve seen that before about clomid and nolva possibly competing or cancelling each other out in other sources. Always surprised when guys still recommend both concurrently for PCT.

6

^i suppose the info can get overwhelming, or guys are used to planning cycles based off what they can get easily, vs what they need.

7

More thoughts on Aromasin: dosage recommendations vary from 25 mg/ED to 12.5 mg/ EOD…

this has a pretty fast half-life (9 hours or so. in contrast, tamoxifen has a rather long half-life (5-7 days) ), so adjusting dosages can be done relatively quickly and easily. i’d start high (25 mg/day), and go from there…

one needs to recall that tamoxifen binds to the estrogen receptor. aromasin is an irreversible steroidal inhibitors, and forms a permanent and deactivating bond with the aromatase enzyme.

since aromasin is an irreversible aromatase inhibitor, there should not (theoretically) be any estrogen rebound. as long as testosterone isn’t absurdly high, estrogen should simply aromatise at a normal rate. the aromatase enzyme that has been deactivated by aromasin will remain that way. (however, letro and a-dex are reversible…)

if you stopped both of these at the same time in PCT, then not only would estrogen be able to attach to the ER, this would also occur at the same time that overall estrogen levels began to rise due to cessation from the AI.

based off this information, i would run PCT similar to this:

8 week test prop cycle
PCT:
Week 9-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 10-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 11-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 12-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 13-Aromasin (25 mg/day)

12 week test enanthate cycle
PCT:
Week 13-Aromasin (25 mg/day)
Week 14-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 15-Nolvadex (20 mg/day), Aromasin (25 mg/day
Week 16-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 17-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 18-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 19-Nolvadex (20 mg/day), Aromasin (25 mg/day)
Week 20-Aromasin (25 mg/day)

(if 25 mg/day of aromasin is too high, then one would taper down as needed, obviously)

http://press.endocrine.org/doi/full/10.1210/jc.2003-031279

8

Makes sense. A couple of questions though (I have no experience with AAS so these questions arise only from my rationale)

  1. Wouldn’t it be a good idea to taper off the SERM to further reduce the possibility of an E2 rebound? This seems to be standard practice among TRT guts attempting a SERM restart. Is this a moot point given the use of an AI during the PCT? Some say that SERMs increase intratesticular levels of E2 and that AIs do nothing for this. If this is true then I guess it would make sense to taper the SERM to avoid the rebound.

  2. What if the rebound is not only a consequence of the uncoupling of a reversible AI, like Arimidex, to the aromatase enzyme as concentrations of the drug drop when it is not taken anymore, but also a consequence of an up-regulation in the production of the enzyme that occurs when the Ai is taken? If this is the case then could a E2 rebound be expected while production of aromatase returns to normal?

9

[quote]eaboadar wrote:
Makes sense. A couple of questions though (I have no experience with AAS so these questions arise only from my rationale)

  1. Wouldn’t it be a good idea to taper off the SERM to further reduce the possibility of an E2 rebound? This seems to be standard practice among TRT guts attempting a SERM restart. Is this a moot point given the use of an AI during the PCT? Some say that SERMs increase intratesticular levels of E2 and that AIs do nothing for this. If this is true then I guess it would make sense to taper the SERM to avoid the rebound.

  2. What if the rebound is not only a consequence of the uncoupling of a reversible AI, like Arimidex, to the aromatase enzyme as concentrations of the drug drop when it is not taken anymore, but also a consequence of an up-regulation in the production of the enzyme that occurs when the Ai is taken? If this is the case then could a E2 rebound be expected while production of aromatase returns to normal?

[/quote]

interesting points.

well, i’m not an expert in chemistry, but i’ll try to reiterate a few things…

  1. most SERMs (with the exception of raloxifene) have a really long half-life, like 5-7 days. a taper is not harmful, but something i would think is generally quite unnecessary, at least for people who use a single SERM, and at the recommended dosage. besides, the SERM doesn’t decrease estrogen, but prevents it from binding to the estrogen receptor…

  2. i can’t really say as for as “up-regulation” is concerned, but if it does occur with the ER, then it should with every other hormone, to the point of the body of removing all “unnecessary new muscle” (in particular, any cortisol receptor, etc)… but more importantly, an estrogen rebound would only occur if testosterone levels were extremely high and so were aromatase levels. the body still requires testosterone levels to be seen as high to make conversion necessary. And if you use Aromasin over Armidex, you wouldn’t see a rapid conversion back in aromatase, but a gradual increase to normal levels, as the body needs to build that enzyme again.

Now, i will admit, i could be wrong on the timing of ending the SERM vs the AI in PCT, but at this time, i don’t see how. if ER is up-regulated, then i’d say i’m still correct in this assertion, as you stop the SERM use while the AI is still being used, so even if the ER is more receptive to estrogen, there’s minimal estrogen to actual fit in to the receptor.

just my .02

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^with that being said, i think it brings up several OTC supplements that would be quite useful in PCT as well (ZMA, d-aspartic acid, PS).

11

Regarding the proposed PCT plans laid out I was just thinking that if the half-life of Nolvadex is 5-7 days then, wouldn’t it be wise to keep taking Aromasin for at least another week after stoping Nolva to assure one doesn’t stop taking it exactly when concentrations of Nolvadex are dropping to a level where they no longer effectively prevent E2 from binding?

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[quote]eaboadar wrote:
Regarding the proposed PCT plans laid out I was just thinking that if the half-life of Nolvadex is 5-7 days then, wouldn’t it be wise to keep taking Aromasin for at least another week after stoping Nolva to assure one doesn’t stop taking it exactly when concentrations of Nolvadex are dropping to a level where they no longer effectively prevent E2 from binding?[/quote]

i was kinda thinking that as well… i don’t know how much it really matters, to be honest. as long as you’ve been on Nolva and Aromasin long enough to lower estrogen and normalize testosterone levels, there shouldn’t be a massive increase in estrogen, and essentially a return to baseline levels.

i think the key is to look at the estrogen issue as a whole. the Nolva prevents E from binding to the receptor. the Aromasin prevents from estrogen being formed. as the drugs are stopped, the ER could have estrogen attach to it, and estrogen could be created from testosterone via aromatization. however, we still need a reason for the body to see the testosterone levels as being too high.

^with this being said, i think you have a valid point, and don’t see an issue with taking the Aromasin for an extra week.

EDIT: so, after typing all that, i found this study: http://jnci.oxfordjournals.org/content/95/11/779.abstract?ijkey=28ff3cf884c4142d414e39f147ad83e37321ed33&keytype2=tf_ipsecsha

apparently, 1 mg, 5 mg and 20 mg doses had comparable effects on reducing the gene expression on the ER. i would think, based off the the half-life of Nolva and off the normal parameters for clearance for tamoxifen, then it doesn’t matter… blood levels should still be around 1 mg 20-28 days later… personally, i’d still go with the original plan i had there.

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I’m going to stick with nolvadex for my pct. What’s your thoughts on these dosing examples.

40/40/20/20

40/40/20/20/10/10

20/20/20/20/10/10

Thoughts, advice?

First cycle: Test e 500mg a week (pinning 250mg twice a week)

.25mg adex eod, more if needed. Should I start adex first day of starting cycle?

14

[quote]Bdubbs wrote:
I’m going to stick with nolvadex for my pct. What’s your thoughts on these dosing examples.

40/40/20/20

40/40/20/20/10/10

20/20/20/20/10/10

Thoughts, advice?

First cycle: Test e 500mg a week (pinning 250mg twice a week)

.25mg adex eod, more if needed. Should I start adex first day of starting cycle?[/quote]

to be honest, i have not seen anything that indicates to me that high doses of tamoxifen are gonna help the HPTA recover any faster. like i said above, the key is simply to get the body used to producing LH and test again.

also, based off the above comparisons on Aromasin to Armidex, i’d go with Aromsin, due to the benefit in PCT, and the fact that it’s much faster acting.

15

[quote]cycobushmaster wrote:

[quote]Bdubbs wrote:
I’m going to stick with nolvadex for my pct. What’s your thoughts on these dosing examples.

40/40/20/20

40/40/20/20/10/10

20/20/20/20/10/10

Thoughts, advice?

First cycle: Test e 500mg a week (pinning 250mg twice a week)

.25mg adex eod, more if needed. Should I start adex first day of starting cycle?[/quote]

to be honest, i have not seen anything that indicates to me that high doses of tamoxifen are gonna help the HPTA recover any faster. like i said above, the key is simply to get the body used to producing LH and test again.

also, based off the above comparisons on Aromasin to Armidex, i’d go with Aromsin, due to the benefit in PCT, and the fact that it’s much faster acting.
[/quote]

Also, according to the first post, the duration of the PCT should be more or less the same as the duration of the cycle, correct?

OP: how long did you say your cycle was going to be? I think this factor would determine whether the above stated protocols are sufficient.

16

[quote]eaboadar wrote:

[quote]cycobushmaster wrote:

[quote]Bdubbs wrote:
I’m going to stick with nolvadex for my pct. What’s your thoughts on these dosing examples.

40/40/20/20

40/40/20/20/10/10

20/20/20/20/10/10

Thoughts, advice?

First cycle: Test e 500mg a week (pinning 250mg twice a week)

.25mg adex eod, more if needed. Should I start adex first day of starting cycle?[/quote]

to be honest, i have not seen anything that indicates to me that high doses of tamoxifen are gonna help the HPTA recover any faster. like i said above, the key is simply to get the body used to producing LH and test again.

also, based off the above comparisons on Aromasin to Armidex, i’d go with Aromsin, due to the benefit in PCT, and the fact that it’s much faster acting.
[/quote]

Also, according to the first post, the duration of the PCT should be more or less the same as the duration of the cycle, correct?

OP: how long did you say your cycle was going to be? I think this factor would determine whether the above stated protocols are sufficient.[/quote]

i think you could run nolva/PCT shorter, but no less than half the length of the cycle. it’s just that i stumbled into some research that showed tamoxifen/toremefin both continue to elevate testosterone for 3 months or so…

17

A synopsis:

HPTA:

The hypothalamus produces gonadotropin-releasing hormone (GnRH). The pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the testes produce testosterone. The body converts testosterone into estrogen by aromatization.

SERMS to use:

  1. tamoxifen (Nolvadex): 20 mg/day-best at raising total LH and test, as well as for a longer duration, and does not increase SHBG
  2. toremifene: 60 mg/day-lowers prolactin more than the other SERMs, does not have the same cancer concern as Nolva, increases HDL (good cholesterol)
  3. raloxifene: 60 mg/day-has a higher affinity for the ER than the other SERMs, and a half-life of only a day or so (vs 5-7 days of nolva, tore and clomid).

distant #4. clomiphene: 50 mg/day-much weaker than Nolva… 20 mg of Nolva is comparable to 150 mg of Clomid. also, Clomid decreases the sensitivity to GnRH.

Aromatase Inhibitor:

Exemestane (Aromasin): 25 mg/day-does not decrease blood levels of SERMs like Armidex and Femara do. also, it has a faster half-life, which makes adjusting the dose easier. Aromasin decreases SHBG, as well…

both Nolva and Aromasin increases test by about 60% individually (Nolva in 2 months, and Aromasin in 10 days), so when they’re combined, one can expect a rather profound effect…

18

[quote]cycobushmaster wrote:
A synopsis:

HPTA:

The hypothalamus produces gonadotropin-releasing hormone (GnRH). The pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the testes produce testosterone. The body converts testosterone into estrogen by aromatization.

SERMS to use:

  1. tamoxifen (Nolvadex): 20 mg/day-best at raising total LH and test, as well as for a longer duration, and does not increase SHBG
  2. toremifene: 60 mg/day-lowers prolactin more than the other SERMs, does not have the same cancer concern as Nolva, increases HDL (good cholesterol)
  3. raloxifene: 60 mg/day-has a higher affinity for the ER than the other SERMs, and a half-life of only a day or so (vs 5-7 days of nolva, tore and clomid).

distant #4. clomiphene: 50 mg/day-much weaker than Nolva… 20 mg of Nolva is comparable to 150 mg of Clomid. also, Clomid decreases the sensitivity to GnRH.

Aromatase Inhibitor:

Exemestane (Aromasin): 25 mg/day-does not decrease blood levels of SERMs like Armidex and Femara do. also, it has a faster half-life, which makes adjusting the dose easier. Aromasin decreases SHBG, as well…

both Nolva and Aromasin increases test by about 60% individually, so when they’re combined, one can expect a rather profound effect…

[/quote]

Nice job! a great follow-up to this would be to clarify HCG and it’s use (when to start and when to stop relative to the cycle, dosing schedule, etc.). Many seem to get confused and start running it for PCT. Others use too much and are not aware of the risks.

19

[quote]eaboadar wrote:

[quote]cycobushmaster wrote:
A synopsis:

HPTA:

The hypothalamus produces gonadotropin-releasing hormone (GnRH). The pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the testes produce testosterone. The body converts testosterone into estrogen by aromatization.

SERMS to use:

  1. tamoxifen (Nolvadex): 20 mg/day-best at raising total LH and test, as well as for a longer duration, and does not increase SHBG
  2. toremifene: 60 mg/day-lowers prolactin more than the other SERMs, does not have the same cancer concern as Nolva, increases HDL (good cholesterol)
  3. raloxifene: 60 mg/day-has a higher affinity for the ER than the other SERMs, and a half-life of only a day or so (vs 5-7 days of nolva, tore and clomid).

distant #4. clomiphene: 50 mg/day-much weaker than Nolva… 20 mg of Nolva is comparable to 150 mg of Clomid. also, Clomid decreases the sensitivity to GnRH.

Aromatase Inhibitor:

Exemestane (Aromasin): 25 mg/day-does not decrease blood levels of SERMs like Armidex and Femara do. also, it has a faster half-life, which makes adjusting the dose easier. Aromasin decreases SHBG, as well…

both Nolva and Aromasin increases test by about 60% individually, so when they’re combined, one can expect a rather profound effect…

[/quote]

Nice job! a great follow-up to this would be to clarify HCG and it’s use (when to start and when to stop relative to the cycle, dosing schedule, etc.). Many seem to get confused and start running it for PCT. Others use too much and are not aware of the risks.[/quote]

thanks! i keep seeing the same questions over and over again, and thought some of this info might help, along with the links to back the data.

but in all honestly, i don’t like HCG.

for someone who’s done a long or overly suppressive cycle, i’d suggest using Triptorelin instead… just don’t use it too much.

20

^i get why people think HCG is helpful, as it mimics LH and forces the testes to remain active. however, it’s still the last step in the HPTA:

"The hypothalamus produces gonadotropin-releasing hormone (GnRH). The pituitary gland produces luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the testes produce testosterone. The body converts testosterone into estrogen by aromatization. "

i think one serious concern in using HCG too much, is actually desensitizing the testes to LH. we know that excess testosterone sends a negative feedback mechanism, that causes us to stop producing testosterone while on cycle. now by taking HCG consistently, one would logically presume that there would be a negative feedback mechanism to deal with excess LH and testosterone… if we keep taking LH, then we’d have to assume that the body will become less responsive in order to counteract the excess.

Anyway, here’s an interesting study, that’s somewhat applicable:

What’s interesting to me, is the subject uses HCG which brings up “T” levels, but they drop back down for a period of time, and then come back up naturally, after a few months…

21

Interesting article. Yes, the progression of “T” levels during an after treatment is strange. The HCG clearly induced the testes to start producing Testosterone again. During this time the “top” of the HPTA should have remained suppressed. When HCG was ceased the testes were now stimulated anymore so Testosterone levels dropped initially but there was something that made the hypothalamus and pituitary to start working again? Any thoughts? Maybe the pituitary and/or hypothalamus got used to “seeing” LH (HCG, actually) and when it was taken away the contrast made it/them react?

Anyway, any reason not to like HCG aside from people taking too much and making their LH receptors insensitive to LH?

Don’t you think one would do well not to allow the testes to become atrophied? Isn’t it counterproductive to recovery?

Thanks and sorry about all the questions. This discussion is very interesting.