How Miguel & the lab rats do it

So I think by now there’s consensus in most parts of the AAS-using universe, that a proper PCT following a more HPGA suppressive cycle should comprise of a SERM, AI & hCG. Although I have seen newbs ask if using just an AI or hCG will suffice… Rather try a SERM for 4 to 5 weeks, for a single component PCT, if your budget is that scant.

The more commonly available options for SERMs are clomiphene citrate & tamoxifen (I’m not going too deep into explanations which have been repeated to DEATH, on this site & others). SERMs work to restore HPGA function by competitively binding to ERs at the hypothalamus, thereby causing an increase in the secretion of LH. Because, elevated LH stimulates the testes to increase/ restart their production of testosterone, right?

BUT in their dormant & atrophied state, regardless of how much circulatory LH you have, your testes just aren’t fit to respond. Indeed, I’ve read studies where blood tests were taken on test subjects some time after a cycle & LH levels were found to be higher than baseline or on cycle. But testosterone levels had not yet risen. And another study where clomiphene citrate (CC) was administered to a group of young men & another of older men. Prior blood tests showed that LH & FSH were higher in the elderly men. After CC administration FSH & LH rose similarly between the 2 groups. Yet mean serum total testosterone & non-SHBG-bound levels rose by 100% & 304% respectively, in the younger men but only 32% & 8% respectively, in the elderly men (although these are age related differences, I’m sure you see my point about the testes’ ability to act upon elevated LH).

And that is my major critique of every PCT I’ve ever seen; they start you off with a SERM for the sake of increasing T levels via elevated LH when those very same testes will be highly unresponsive for sometime into your PCT (another critique is that conventional wisdom suggests waiting too late to start PCT). Cue the LH analogue known as hCG. It quickly brings your testes back to size & out of dormancy. Instant (short term) endogenous T production. And it elevates T levels for days after administering. My logic tells me that hCG should be introduced towards the end of your cycle, in anticipation of the SERM portion of your PCT. In fact if you’re using, say trenbolone or deca in your cycle, 2 to 3 weeks of hCG during your cycle would serve you well. So during, say a 5 week PCT, you’d start hCG more than a week before you start that SERM (consider day 1 of the SERM as the beginning of your PCT) & stop using it during the 4th week of PCT. Allowing for more than a full week of just the SERM (at the end of PCT) to see where you really are in your recovery & endogenous T production.

BUT you can’t just use that hCG willy nilly. 1stly, the more testosterone there is, the greater the amount of aromatizing that occurs. 2ndly hCG has the ability to increase aromatase activity in the Leydig’s cells, leading to even more oestrogen production. So for the above reasons & also for the sake of negative feedback manipulation (everything mentioned thus far has been for the sake of manipulating factors involved in negative feedback), we introduce an AI. Because basically, the body’s assumption is that high levels of oestrogen detected are a result of high levels of T which has been aromatized. Under natural conditions, more T equals more oestrogen, in the ratio applicable to each individual.

(Physiologically, 80% of circulating oestrogen in men is produced by the aromatase pathway. The remaining 20% is produced directly by the testes)

Just a quick recap: for the less suppressive or shorter cycle, a SERM should suffice. Otherwise go for a SERM, hCG & an AI. You’d then first decide which SERM to use. Followed by the toss up between urinary hCG & recombinant hCG. Then finally, the AI. Should you opt for CC, no limits. But if it’s tamoxifen you want, then your only option is exemestane.

Now for an effective PCT you need to create the smoothest transition from cycle to natural training. Besides retained water, the main culprit for loss of gains is that dip/ absence of anabolic hormones between your last injection & eventual resumption of endogenous androgen production.

So here’s what I do: besides suggesting low to moderately doses during the cycle, the very last injection of a long estered compound would be of a lower quantity eg. for TC 300mg (some people also decide to use short estered or quick acting compunds between that last injection & PCT). Then take the given half life of the compound (12 days for TC) then shave off a few days, coinciding with the day or 2 days BEFORE you would expect (from past experience) to lose strength in the gym &/ or water from decreased oestrogen. For the example of TC, I say 10 or 11 days from your last injection, is when you begin the the SERM, at a dose that will allow it to become active sooner in your body (exogenous androgen levels at this stage won’t be enough to suppress your recovery). But remember what I said earlier about not allowing that dip in your anabolic hormone levels? You’d have also began hCG more than a week before that, achieving good T levels even this far after your last injection. Simultaneously, your testes are now also more responsive to the LH being released as a result of the SERM & AI.

So for some time since your last injection until your 2nd last week of PCT, thanks to hCG, you’ve got GUARANTEED endogenous T, holding onto those gains, smoothing the transition. But using high doses of hCG, for extended periods of time, desensitizes the testes to endogenous LH. Also, using doses that are too high means that the overly elevated T will suppress its own production… Ok so, for the last 1 to 2 weeks of your +/- 5 week PCT, you’re cruising on a SERM & AI only. And at the lowest doses possible.

With a good diet, nutrition, training regimen, rest/ sleep etc I see no reason why anyone should lose anything more than retained water after a cycle, even without access to MSRP.

Before I forget, could someone please explain the logic behind using CC & tamoxifen together for me, please. A link to a study or 2 or even the theory behind it will suffice for me.

I’ve tried out several combinations on the SERM-AI-hCG PCT format on both MSRP groups (experiment) & non-MSRP groups (control). I won’t bother mentioning the experiment group’s results coz that’s just not fair. For the control group, the least that’s been lost after an 11 week bulking cycle, was 0,5kg, a result which I’ve repeated.

One PCT combination I’d never tried before was: CC, urinary hCG & letrozole. But currently, that’s what I’m doing with a certain subject. So n=1 for that i.e. it’s a case study. I’ve attached it as an example. What I originally had sat down & planned is different from what has actually happened. For example, he began the letrozole too late (other issues) & consequently ran higher doses than I would have preferred at that time of the cycle, to allow active, circulatory levels of the drug to rise sooner. Plus, I would’ve preferred 2 more hCG injections near the end. So I’ve given what has happened (& is still going to), rather than my original planning. He’s on MSRP & his cycle looked like this:

Week 1-3: 400mg TC
Week 4-9: 500mg TC
Week 10: 325mg TC

I’m 90% certain that week 4-9 at 400mg would have produced the same end results, as long as my diet & training guidelines were followed, even taking into consideration increased cortisol resulting from the supraphysiological T levels. But, we had 2 vials to finish… I’ve NEVER seen letrozole used as part of PCT before.

I know that I said I would reference most of what I’ve said & I haven’t. But, if anyone wants something referenced, simply request I support any quote I’ve made. It is now 02:37. Gonna haul my insomniac self off to bed now, then paste this into as.co.za sometime when I wake up. Goodnight

POST SCRIPT: Upon my (self-serving) suggestion that my friend use letrozole as the AI for his PCT, his response was that it would be a waste since it takes 60 days (at 2.5mg daily or 30 days at 0.5mg daily) for letrozole to reach stable blood levels and his PCT wouldn’t even last one month and a half. True. But on a similar note, people who I’ve assisted in treating gynaecomastia using letrozole, have lost their libido, while on T, within 4 days (tapering from 0.5mg, 1mg, 1.5mg to 2mg). And again, it takes about 4 to 5 weeks to reach stable plasma levels of TC. So how does he explain his having gained 2kg just in his 1st week?! Followed by a total of 9kg by his 5th injection?

The answer is simple enough. Even if plasma levels of a drug haven’t stabilized, doses do still produce the peak & trough effect. For example, TC takes 24 to 48 hours for plasma concentrations to peak. Following which, they gradually decline back to baseline ( www.medibolics.com/freq2.htm ). Each drug has it’s own unique peak-trough graph & time frames thereto. No points for guessing how & why stable blood levels are eventually reached …

Ok, NOW I’m really off to bed!

Miguel, read below for the details between both the compounds, however the second link compliments the use of Clomid and makes a good point why it's important.

www.101steroids.com/index.php/2010/02/no...e-citrate-tamoxifen/

www.ironmagazineforums.com/anabolic-zone...ex-together-pct.html

Enjoy

Hmmm... I won't comment on the 1st link since it didn't tell me anything I don't already know, especially something which would be material to the question of what synergy/ positive interaction exists between CC & tamoxifen.

And I don't think Dr Scally (as much as I admire his work, most recently that article on equal prolactin increases from exogenous T & nandrolone) answered the question satisfactorily or at all. He mentioned nothing new or little known. Except perhaps in his 2nd paragraph where he pointed out that CC is a mixed agonist/ antagonist for the ER. Something which can in fact also be said of tamoxifen. Hence the letter S (for "selective") in SERM. And also the ability of CC to sensitize pituitary cells to the action of GnRH/ LHRH. Implying that CC would cause greater amounts of LH to be released from the pituitary for the purpose of exerting favourable effects on the testes, right?

Now given this superiority of CC at causing a higher pituitary sensitization to GnRH, still, 150mg of CC is required to produce the same increase in LH, FSH & T as just 20mg of tamoxifen.

But all of the above is neither here nor there. There are several studies on both CC & tamoxifen, showing positive results in the parameters which are of interest to us. That point was never up for debate. After all, the PCT I attached above makes use of CC.

If you'd like to see an example of how drug interactions for clinical treatment are concluded upon, check out the ATAC (anastrozole, tamoxifen alone or in combination) trial. As the name suggests there were 3 groups under observation. The 1st being treated with anastrozole only, the 2nd with tamoxifen only & the 3rd with a combination of the 2. Each group had more than 3000 individuals, under observation over several years. They QUANTIFIED the results/ treatment outcomes for each of the 3 groups & stated the p-value for each given outcome between the 3 groups.

In the end Dr Scally mentioned that adding tamoxifen "seemed" to improve the clinical response. Whereas he could've taken objective measurements of LH, FSH, free T, non-SHBG-bound T etc. he decided to go for more subjective feedback. Subject to observation bias among other things.

The best way to eventually conclude whether you're really getting any benefit from using CC & tamoxifen simultaneously would be to run trials (on a sufficiently large n) using just 1 drug at a time & then both. Of course, without violating the ceteris paribus assumption.

Otherwise, doing the whole CC 1st then tamoxifen dance is just a waste of money if you're only getting equal or lesser results. Or just because it "feels" better. Something which you wouldn't be able to comment on anyway, unless you'd done the same PCT prior with the simultaneous, use of those compounds being the only change made. Hence isolating the responsible variable.

@pump Thanks for the read.

Thats why you will see in my older posts I only mention the use of tamoxifen in PCT and myself and Inja both agreed that tamoxifen is the more pure SERM and Clomid in not needed in PCT. However the Doc mentions its use, however I was not on the forum in his time to actually fully understand he reasoning. Ill try dig up what I can, and would appreciate if you did the same. This is what I enjoy, these indepth understanding of different drugs, and not just shallow answers without scientific evidence.

Very good read! Nicely explained.

2 requests:
Please go slow on acronyms and WTF is MSRP?

BTW - i'm convinced that using HCG during cycle is a must - whats your views on that?

Also
Letro killing libido in 4 days? i can vouch for that. I stopped after a week and 4 weeks after i still struggle a bit on the third round. :laugh:

jackrabbit1 wrote: Very good read! Nicely explained.

2 requests:
Please go slow on acronyms and WTF is MSRP?

BTW - i'm convinced that using HCG during cycle is a must - whats your views on that?

Also
Letro killing libido in 4 days? i can vouch for that. I stopped after a week and 4 weeks after i still struggle a bit on the third round. :laugh:

There are lots of guys here dying to find out what MSRP is
I can also vouch for the Letro. It turned me into a eunuch inside a week!

Thank you Miguel for the read but my only request is to maybe dumb it down slightly for us less biologically inclined folks! But I think I understood what you were saying.

This just in:

forum.mesomorphosis.com/steroid-forum/2-...les-134287264-7.html

Page 7 onwards is what you ought to be interested in. Haven't read it myself, just skimmed some key words

As of Sunday, February 6th, I instructed my friend to administer 0.1mg of letrozole daily, instead of E2D. Besides having made more gains (he's now between 97kg & 97.5kg), he informs me that his libido has increased as well. The one thing that I still think needs alteration on the PCT attached above is the dosing for letrozole. I'm curious to find out how much higher I can safely prescribe it, in correspondence to the different stages of a PCT.

I'll find out soon. Yesterday, another subject of mine did the 8th injection of [technically] his 1st cycle. Started at 82kg, he's now sitting at 98kg. 2 more injections remain, following which he commences his letrozole-hCG only PCT.

Coming from a background where I'd only used letrozole for the treatment gynaecomastia, I'm well aware & always wary of what effects it might have on libido (considering that PCT is, after all, a treatment of sorts for secondary hypogonadism). But, letrozole has successfully been used not only for breast cancer treatment, but also as a fertility treatment, for hypogonadism & to slow bone maturation, amongst other things. And with favourable effects, in humans, on IGF-1.

So yes, I'll be omitting the SERM from the above mentioned SERM-AI-hCG format for a PCT. But, both SERMs & AIs are manipulators of negative feedback wrt the HPG-axis. Which is why both have been used as fertility treatments. The principle difference though, is that SERMs create a PERCEIVED lack/ absence of oestrogen, whilst AIs create an ACTUAL lack/ absence of aromatized oestrogen. Let's also bare in mind that oestrogen is an anabolic hormone, so the libido effect isn't the only thing to watch out for with letrozole.

In this coming PCT though, I'll have 10000IU of hCG to work with, as a libido safety net, while I do the upwards adjustments for the letrozole dose.

Did anyone read my previous link? It would seem the assertion that oestrogenic activity at the pituitary sensitizes it to LHRH/ GnRH is based on oestrogen priming. Something which does not occur in males. In fact, quite the opposite applies for males i.e. oestrogenic activity at the pituitary causes desensitization to LHRH.

Which once again leaves us with the question of why use BOTH tamoxifen & CC during PCT?

Miguel, I honestly have not found evidence to say otherwise they both triphenylethylene compounds and are both classified as a SERM... As reports stated 20mg of Nolva in 10 days yielded a 142% of baseline increase in testosterone that being the same results yielded on 150mg of CC.

The more sensitive the pituitary is the more luteinizing hormone will be released the higher the increase in testosterone. Studies again show the Clomid actually lowered the sensitivity after 10 days while Tamoxifen increased sensitivity still at 6 weeks.

So in men I don't see how CC can be more effective or is even necessary? Yes for women CC has better affirmation on the ovaries as opposed to that of Tamoxifen (well so it’s said) which works better on peripheral tissues, however being men and speaking about PCT I doubt we need to worry about that very much.

Im in agreeance to higher Testosterone levels experienced while on Nolva, Im on day 12 of Nolvadex in my PCT regime have not included Clomid and my strength yesterday was as if I was still on Testosterone. I benched 150kg 8 reps clean to the chest and back up which is what I usually do whilst in the middle of a cycle. I was stunned. Started my PCT precisely 3 weeks after my last shot of Cyp 500mg. Letrozole was used at 6 drops EOD throughtout cycle, tapered down to 3 drops EOD, then used HCG instead of Clomid 1000iu Day 1, 1000iu Day 2, 1000iu Day 3, Week 2 1000iu, Week 3 1000iu. Nolvadex Started week 2. in week 4 now.

00pump wrote: Miguel, I honestly have not found evidence to say otherwise

is this with regards to my question of the necessity of both CC & tamoxifen within a PCT regimen? i.e. you're merely agreeing

00pump wrote: So in men I don't see how CC can be more effective or is even necessary?

the question of the more superior SERM was never really up for debate, in fact i had affirmed tamoxifen the victor, on a mg per mg basis etc from the outset. but, you cannot summarily declare CC useless. the studies are there to support its effectiveness in eventually increasing T levels. i for one have a preference towards tamoxifen, but this won't deter me from making use of it in situations where tamoxifen would not be a viable option. for example, the abovementioned PCT where letrozole was used.

i find myself quite intrigued by this AI. i have yet to see another with similar potency in not only aromatase inhibition, but it's ability to increase T (T was elevated to supraphysiolgogical levels in several of the participants of a certain study i've encountered www.eje-online.org/cgi/content/full/158/5/741 ), IGF-1 etc. so like i said, i've got a PCT coming up which will include letrozole & hCG only.

just to reiterate a statement i'd previously made, "oestrogen priming... does not occur in males. In fact, quite the opposite applies for males i.e. oestrogenic activity at the pituitary causes desensitization to LHRH."

Correct.. I'm saying I don't see the reason for using CC + Nolva.

Secondly, yes the above mentioned PCT can and will work, however the CC + Letro can be replaced with Nolva + Letrozole as the whole point of the Letro would be to prevent the negative feedback loop associated with estrogen and aid in recovery of the HPTA. I find I experience far more severe sides like "hot flashes, cramping, blurred vision" while on 100mg CC and very rarely experience this while on 20mg/pd of Nolva, Letro can even be associated with these side effects, but once again even at 2.5mg a day of Letro I don't seem to suffer hot flashes or blurred vision, however I do experience extremely dry joints and 0 Libido for weeks after discontinued use of the drug, then again that is my own fault for not allowing enough estrogen. Again another option that aids in boosting Libido is suppressing progesterone, and as much as this hormone boosts Libido in women, it can completely cripple a man.

What dose are you going to be using for the Letro + hCG PCT ? 0.02mg Letro ED. What is the halfe life here, 48 hours? Also when are you starting the Protocol or are you just using Letro during cycle + through into PCT ? I see some studies provide a 45% increase in testosterone in just over 2 days in their trials. And I see data provided on Letro was higher on the LH hormone levels in elderly and young males compared to other male fertility trails that where carried out using Clomid / and Nolva.

Also using Letro you will be able to increase the hCG dosage without worrying about other potential sides resulting from elevated estrogen levels, but I would guess you would need to run it and tapper off at the end to prevent any rebound effect from the hCG and adjust dosage accordingly to potential side effects, that is the only thing with Letro that will be difficult if you don't tapper off and you are using higher doses 0.25/0.5mg etc, ED / EOD you might have that rebound effect and again suffer from Libido issues when Free estrogen flares up.