Cycle Regimen Critiques

Lol, my stance on pct is that it's pointless to do if you plan on using gear for a long period of your life. If you're just dabbling then by all means pct is OK. If you want to push the envelope and see what your body can really do, then pct isn't going to allow that.

Now then, as for waiting for the circulating compounds to dwindle in the blood is for a good reason. The body won't start producing test again, even when coerced with a serm, unless circulating androgen levels are below normal.

Negative feedback: Low circulating androgens or a SERM/AI negating an estrogenic response..??

Regarding PCT, if you believe you have the genetics that may one day put you on a podium position of a major bodybuilding federation, then by all means go for cruise-blast...

If you are like most people, genetically mediocre and you just wish to be bigger via supraphysiological doses of hormones, and don't care about your future health, then cruise-blast is your choice, if you should wish to make that decision..

I believe CFC and myself have put forward a strong case for stating long term supraphysiological doses of hormones are detrimental to cardiac health...

If longevity of life is your primary concern, then the greater time your body is free from the effects of large doses of exogenous hormones the better.. That is why some people choose PCT, it might not be the optimum protocol for maximal growth potential, but if correct nutrition and training methodologies are followed losses can be minimised.

I suppose it depends on the individual, but as your heart starts to give cause for concern in your 40-50's (or earlier in some people), remember one thing, you can't go back and undo the decades of damage..
You will ultimately have to live (or die) with your decision, so choose wisely..!!!
 
@gf
Couldn't tell if you were saying I was incorrect or not so I'll ask lol. I thought even with serm usage, if circulating androgen aren't low enough, the body still won't restore test production?if memory serves right, the serm tricks the body into producing test because it thinks estrogen levels are low and in the male body, our key method of estrogen production was via aromatase.
Also wanted to ask about using Aromasin in place of adex as I saw Aromasin itself has actually been shown to boost natural test levels and is more kind to the body: not affecting lipids and actually boosting IGF 1 levels which woukd he beneficial when exogenous supraphysiological androgen are declining. Also no estro rebound when discontinued. Just curious.
 
@gf
Couldn't tell if you were saying I was incorrect or not so I'll ask lol. I thought even with serm usage, if circulating androgen aren't low enough, the body still won't restore test production?if memory serves right, the serm tricks the body into producing test because it thinks estrogen levels are low and in the male body, our key method of estrogen production was via aromatase.
Also wanted to ask about using Aromasin in place of adex as I saw Aromasin itself has actually been shown to boost natural test levels and is more kind to the body: not affecting lipids and actually boosting IGF 1 levels which woukd he beneficial when exogenous supraphysiological androgen are declining. Also no estro rebound when discontinued. Just curious.

I was asking a question as I was too lazy to double check..lol

I would agree with your statement on aromasin...
 
Okay... Sorry for taking so long to respond to this but things have been busy at work lately. My question wasn't whether or not to complete PCT or your opinion on this matter, but rather just why I should wait between the end of my cycle and PCT.

Just to preface this... I know there's a lot of testosterone pumping through most of the people reading this forum. That being said, I'm not trying to sound like I'm preaching at you or attacking you and I understand that everyone has a different approach to how they prefer to use AAS and that's perfectly fine; it's your body, do as you please. What I am trying to do is give others a firsthand account of my experience with refusing to use a PCT program while also providing some education to those who are interested as to why PCT is a health-conscious decision that can be beneficial for their future. Sometimes, preventative measures are important for ensuring good quality of life down the road... Take the necessary precautions now and don't end up regretting your decisions later. Of course, this is all assuming that you're not going for your IFBB pro card trying to be the next Mr. Olympia.

Lol, my stance on pct is that it's pointless to do if you plan on using gear for a long period of your life. If you're just dabbling then by all means pct is OK. If you want to push the envelope and see what your body can really do, then pct isn't going to allow that.

Now then, as for waiting for the circulating compounds to dwindle in the blood is for a good reason. The body won't start producing test again, even when coerced with a serm, unless circulating androgen levels are below normal. Otherwise the negative feed back loop is active in the sense: high androgens, no more test is needed, nuts still shut down. Once levels get low enough then the body recognizes it needs to start production again. The time before pct begins is all based on the active life of the drugs in the body. Dropping longer esters like cyp and enanthate a couple weeks out allows blood levels to drop, but also means progress will stall out, gains may begin being lost although minimally. So the idea is to substitute in short life drugs during the time the longer active drugs are leaving the body. This can be done with injectable like test prop/ace/pp or with orals. This allows you to bridge that time so that the amount of time spent with low hormones is minimal.


1.) My experience with not implementing a PCT program: I am estrogen sensitive and a long time ago, back in one of my previous cycles I actually did just what you suggested because I was naive at the time and my friend suggested not completing any PCT either... I was on 750 mg/week of Testosterone Enanthate and 150 mg/week of Trenbolone Acetate... I followed a simple taper off design and didn't complete any PCT. Well... guess what? A few weeks later I absolutely blew up... not in a good way. I was bloated, breathing heavy, retaining huge amounts of water and gaining large amounts of fat. I went from dry and lean to looking like a puffer fish... My face was red and swollen and it basically looked like I was constipated all the time... haha. I decided to get some bloodwork and sure enough my estrogen levels were through the roof, my testosterone levels were at the very bottom end of normal, and my liver enzymes were... well let's just say "not optimal". I went from 265 lbs at 11% body fat to around 255 lbs at 18% body fat in a matter of 2 months (these numbers are verified by DEXA just in case you were wondering)... training stayed the same and diet on point. Not to mention that I also had gyno issues post cycle as well with a few small knots developing and then luckily, after some time disappearing. Had I have implemented a proper PCT cycle, I'm sure that I would have retained a large amount of my gains (although some loss is inevitable) and I definitely would not have bloated up like an airbag due to my ridiculous estrogen levels.

2.) Clomiphene, as I'm sure you are well aware stimulates the release of GnRH from the hyopthalamus which then triggers release of FSH and LH from the anterior pituitary, causing the testes to produce testosterone... and yes, to a certain degree this does happen even when serum testosterone levels are augmented. However, this doesn't occur with other SERMs such as Tamoxifen, this is well documented in the literature. Beyond this, however, using a SERM directly after cycle would help with, if not prevent to some degree, estrogen rebound. I understand that it is "all about the T to E ratio" but, as your testosterone levels begin to drop, that doesn't necessarily mean that your estrogen levels drop as well in a linear fashion with testosterone. In fact, it's more likely that as your testosterone levels decline, your estrogen levels, while beginning to decline, do so at a slower rate. So, waiting the length of the half-life of whatever compound you're taking to begin PCT can theoretically be detrimental. Granted, your T to E ration could still be favorable, however, this doesn't negate the fact that if you're estrogen sensitive, you're still going to develop tremendous estrogenic side-effects from elevated estrogen levels. Hence why I'd consider starting PCT (at least some sort of SERM or AI) directly after the end of my cycle. Testosterone is still being converted to estrogen, but estrogen levels are declining at a slower rate and as such, at a certain point, without any AI or SERMs, your estrogen levels actually end up being higher than testosterone levels after a couple of half-lives (assuming you don't start any PCT and don't cruise in-between cycles). Obviously, having your T to E ratio flipped is not desirable.

3.) As someone with an extensive background in physiology I can assure you that PCT is indeed helpful... unless of course you plan on taking supraphysiological doses (even at a low dose of 200-400 mg/week it's far more than your body produces naturally) of exogenous hormones for extended periods of time (i.e. years...) which is extremely recommended against from a health standpoint. I understand the mentality behind the cycle and cruise concept for competitive bodybuilders that do this for a living... but for the person that values living to see their grandchildren over vanity (assuming again this isn't where someone derives their income from), PCT is a necessity. Plenty of gains have been retained, losses have been minimized and progress has been made while following a cycle on, PCT, short break interval and cycle on again; personally, I'm okay with losing a small amount of my gains to save my life later down the road. Not trying to preach at you, but after having held plenty of cadaver hearts that are the size of a small child and reading bloodwork with unbelievably high liver enzymes, cholesterol, etc. due to excessive exogenous hormone use... I'll stick with implementing a PCT protocol. I'm not making my income off of being a competitive bodybuilder, this is just an in-depth hobby for me and something I truly enjoy doing. Now, if this is your source of income and you are at a point where you believe you could be the next Jay Cutler or Phil Heath, then by all means do whatever necessary to become the best... just realize the expense it comes with.

Okay... I think that covers that. Again, not trying to argumentative but just trying to offer some experience and knowledge to those who are interested, not trying to command anyone to do anything... haha.
 
@gf
Couldn't tell if you were saying I was incorrect or not so I'll ask lol. I thought even with serm usage, if circulating androgen aren't low enough, the body still won't restore test production?if memory serves right, the serm tricks the body into producing test because it thinks estrogen levels are low and in the male body, our key method of estrogen production was via aromatase.
Also wanted to ask about using Aromasin in place of adex as I saw Aromasin itself has actually been shown to boost natural test levels and is more kind to the body: not affecting lipids and actually boosting IGF 1 levels which woukd he beneficial when exogenous supraphysiological androgen are declining. Also no estro rebound when discontinued. Just curious.


I'd be careful with Aromasin, only because it's a suicide aromatase inhibitor... and by this I mean it bind irreversibly to the active site of the enzyme rendering it inactive... Some conversion of testosterone into estrogen is a good thing. This is why it's used in advanced breast cancer after treatment with Tamoxifen has failed and breast cancer has continued to progress. To answer your question, it has been shown, along with Clomiphene to induce testosterone production... although to a lesser degree. The effects of Aromasin on IGF-1 are actually inconclusive. In women I think it increased IGF-1 something along the lines of 0.28% but on a study in young men there was no change observed in plasma lipids or IGF-1 levels. [1]

Hope that helps clarify some of your questions.

[1] Pharmacokinetics and dose finding of a potent aromatase inhibitor, aromasin (exemestane), in young males. J Clin Endocrinology Metab. 2003. http://www.ncbi.nlm.nih.gov/pubmed/14671195
 
DNP [Mod-Edit.. you need to alter your tone young man, I'm starting to lose patience]..... 1.) Don't be surprised if you get cataracts and go blind. Anything that works in the timeframe this garbage does is very dangerous. 2.) The more extreme the results, the more you pay the price with your health. 3.) Molecular neurobiologist... in other words no future in physique business... all the guts but no glory in the end.

Okay... I wasn't going to reply to this but I guess I will. As I always preface my posts that could be taken as authoritative/argumentative, not trying to start an argument but just trying to present some facts... do with them what you will.

1.) I understand the risks associated with DNP... please read more literature on this substance. I am not out to promote its use, but I am going to document my experience with for others who are interested. Now... on to the cataracts. If you had read the literature, you would understand that the development of cataracts has been documented in the use of DNP by females. There have been, if I can remember correctly, less than 3 (someone please correct me if they know the exact number) documented cases of cataract development due to use of DNP in men. I don't believe that these are well documented cases, either. Of course there is anecdotal evidence of cataract development in men from using DNP all over the internet on forums (there's also people claiming to gain 30 lbs of muscle from using "Force Factor" and those that claim they've lost 50 lbs of fat only by using "Hydroxycut") but as far as hard fact-based documented cases in the literature... good luck finding more than one or two. Also If you'll take note, out of the 32 documented cases of cataracts in this paper that developed from DNP use, 100% of those affected were women (they reference 1 male from another study), the average age of use was 45 years old (skewed by a couple of people in their 30's with the majority of the subjects being in their 40's to 60's... obviously there are a lot of free-radicals that have developed in the body by this age) and the average duration of use was 11 months, with the shortest being 3 months (this is excluding time off from the drug, so that's an average of 11 months of either continuous or cumulative DNP use, which is FAR longer than anyone that has their homework would take DNP). [1]

2.) This is correct. However, I would be more concerned with your stance on PCT and the effects of long term administration of exogenous hormones on the cardiovascular system and your liver enzymes. Also, other fat burners such as Clenbuterol and Ephedrine actually pose a greater risk to cardiovascular health and there have been many more documented cases of death due to cardiovascular complications and/or liver toxicity from long term use of AAS without proper PCT as well as Clenbuterol and/or Ephedrine. Not that I want cataracts, but if I absolutely had to choose, I would take cataracts any day over a stroke, heart-attack, or going septic from liver toxicity. Yes, DNP can be toxic, however, if correctly dosed and managed the chances of anything severe happening can be greatly diminished. Once again, not promoting its use, just stating facts. Also, looking into the cases of DNP overdose that resulted in death, you'll find that a large number of them were suicides. [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14]

3.) Maybe you're actually correct with this statement. I am not doing this for the "glory", I'm not an egomaniac. This is a hobby of mine because I'm interested in the physiology behind it, I appreciate helping others, and I also enjoy training and pushing myself to be better on a day to day basis, whether that be through advancing my knowledge, progressing in my career, or improving my physique. I do not have a future in the "physique business" beyond researching said substances and possibly developing something from this. However, you're correct... I'm not looking to be the next Mr. Olympia. I do this because it is a passion of mine but, I don't derive my income from it and it is not my career path... I do believe though, that it's important to educate others about the potential benefits and detrimental effects of what they are putting in their body. If you are on a level of trying to make bodybuilding your career path and either have or are competing to get your IFBB pro card/training to compete with the likes of Phil Heath, Kai Green etc., then more power to you. For most people on this forum, I assume that is not the case... Everyone has their different set of beliefs as to what they're willing to do to get where they're going and the sacrifices they're going to make along the way and that's fine. I'm just here to be a resource to those that are interested and prevent any misleading information from being taken as fact.


[1] Cataracts Following the Use of Dinitrophenol: A Summary of Thirty-Two Cases http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1760503/pdf/calwestmed00398-0029.pdf
[2] http://www.ncbi.nlm.nih.gov/pubmed/15899737
[3] http://www.ncbi.nlm.nih.gov/pubmed/8303802
[4] http://www.ncbi.nlm.nih.gov/pubmed/3381740
[5] http://www.ncbi.nlm.nih.gov/pubmed/11107578
[6] http://www.ncbi.nlm.nih.gov/pubmed/21903417
[7] http://www.ncbi.nlm.nih.gov/pubmed/22104006
[8] http://www.ncbi.nlm.nih.gov/pubmed/12063710
[9] http://www.ncbi.nlm.nih.gov/pubmed/1951424
[10] http://www.ncbi.nlm.nih.gov/pubmed/8497958
[11] http://www.ncbi.nlm.nih.gov/pubmed/19643360
[12] http://www.ncbi.nlm.nih.gov/pubmed/19533818
[13] http://www.ncbi.nlm.nih.gov/pubmed/8045663
[14] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026349/
 
In reference to my pct view: I'm not saying it's pointless. I'm just on the blast and cruise train personally. As I see pct is more of a "weekend warrior" pursuit, and if that's the case I feel one shouldn't even use gear. I feel if one can't make that commitment, then maybe this isn't for them. That's just my view.
 
On that note, how do you even know the true dose of a pill or potion purporting to contain dnp? Do you check each parcel with GC/MS? How do you know the amount of live substance is correct as to what's stated. A very basic very negligible risk. The irony is the answer: your supplier would have a lot of incentive to make sure he didn't kill you and bring unwanted attention on himself. That's the line between overdose and correct dose.

Interesting standpoint you have on PCT... I do have plenty of colleagues that run a typical 12 week cycle, 4-6 week PCT program and 4-6 weeks off and then pick up another cycle that have retained a large amount of gains and are definitely (although yes, after years of cycles and training) still supraphysiological. They may not be Ronnie Coleman big, but I'd call 5'10" 240 lbs and 9-10% body fat pretty dang big... definitely bigger than their body would every allow them to be without using AAS over the years. Anyway, neither here nor there... like we both agree, to each their own.

I agree with the amount of people using ephedrine/clenbuterol... very true. Just from a cardiovascular risk standpoint it's slightly unnerving to me personally... especially if someone with an unknown underlying cardiovascular disorder decided to partake...

Regarding the DNP, I think comparing Heroin to DNP is like comparing apples to zebras... (especially from an addiction perspective) but I do understand where you're coming from regarding purity and knowing exactly what you're getting. Funny you referenced GC/MS as most people don't even know what either of those are; I do use HPLC/Mass Spec and/or Gas Chromatography to verify all of my supplements... fortunately I have access to those machines, as most people don't. As far as knowing my dose, I don't order anything pre-made. Everything I get is in base form/uncapped powder so I do all measurements myself. It's nice having peace of mind regarding what exactly I'm putting in my body. I know people that have ordered some sort of liquid test/tren/deca etc. and end up getting a vial of olive oil...haha... Guess I'm fairly fortunate in that regard.

Thanks for the response man... if everyone had the same opinion the world would be one hell of a boring place. Glad someone can actually respond to a post, disagree and make their statement, and keep things civil... See way too many posts where people would be trying to kill each other if they were actually having the conversation in person. haha
 
2.) Clomiphene, as I'm sure you are well aware stimulates the release of GnRH from the hypothalamus which then triggers release of FSH and LH from the anterior pituitary, causing the testes to produce testosterone... and yes, to a certain degree this does happen even when serum testosterone levels are augmented. However, this doesn't occur with other SERMs such as Tamoxifen, this is well documented in the literature. Beyond this, however, using a SERM directly after cycle would help with, if not prevent to some degree, estrogen rebound. I understand that it is "all about the T to E ratio" but, as your testosterone levels begin to drop, that doesn't necessarily mean that your estrogen levels drop as well in a linear fashion with testosterone. In fact, it's more likely that as your testosterone levels decline, your estrogen levels, while beginning to decline, do so at a slower rate. So, waiting the length of the half-life of whatever compound you're taking to begin PCT can theoretically be detrimental. Granted, your T to E ration could still be favorable, however, this doesn't negate the fact that if you're estrogen sensitive, you're still going to develop tremendous estrogenic side-effects from elevated estrogen levels. Hence why I'd consider starting PCT (at least some sort of SERM or AI) directly after the end of my cycle. Testosterone is still being converted to estrogen, but estrogen levels are declining at a slower rate and as such, at a certain point, without any AI or SERMs, your estrogen levels actually end up being higher than testosterone levels after a couple of half-lives (assuming you don't start any PCT and don't cruise in-between cycles). Obviously, having your T to E ratio flipped is not desirable.

QUOTE]

To bump an old thread... There has been some debate recently on other forums regarding whether Nolvadex or AI's can stimulate LH as part of PCT... As opposed to Clomiphene..

Thoughts pls......

From another site:

Tamoxifen does increase testosterone levels, presumably by inhibiting the negative feedback loop at the level of the hypothalamus. Aromatase inhibitors also increase testosterone, if you are preventing the conversion of testosterone to estrogen then it is only logical that there will be more testosterone available.

http://press.endocri.../jc.2003-031467

Just search tamoxifen + LH it has been researched a lot. It's actually stronger than clomid in it's effect on LH
........
 
Don't have time to do much reading at the moment, but from the top of my head I remember this paper which appeared to show Tamox possibly more effective for our purposes than clomid:

http://www.ncbi.nlm.nih.gov/pubmed/640052

I would naturally assume that an AI would be beneficial by reducing oestrogen conversion during PCT (and thus positively influencing HPTA) and also helping attenuate any negative rebound once treatment with tamox/clomid ceases.

However, I can't say I've really analysed the subject in great depth before. I probably should, though I know there's nothing truly conclusive to be found due to lack of research, and because PCT probably makes little difference for a large number of guys who'd recover anyway, and won't help those using deca much at all.

EDIT: I also remember reading this one more recently, which suggests the Clomid may cause damage to the (rat's) testes in the presence of elevating oestrogen levels (and may be an argument for throwing in an AI)*:

http://www.ncbi.nlm.nih.gov/pubmed/22999797


Oh and there was this one on tamox alone which looked promising (but no comparison with clomid):

http://www.ncbi.nlm.nih.gov/pubmed/6193975

And, just had a quick look for any recent reviews on male infertility, this might be promising from a skim read GF, which is also free to read:

http://www.ncbi.nlm.nih.gov/pubmed/23970453

* I forgot to add, though it's obvious, that this doesn't mean tamox doesn't also do the same. In the literature, the two are basically used pretty interchangeably in studies as 20mg vs 50mg. Ultimately 6% more of this and 12% more of that over a few weeks doesn't make a rats arse of difference over a longer period of time.
 
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This is a link to the paper I was referencing, it is a direct comparison of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

When the effect of clomiphene and tamoxifen on pituitary gonadotropin release was studied, it was found that clomiphene, "unlike tamoxifen, exert[ed] a direct estrogenic rather than antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin."1

1 Disparate Effect of Clomiphene and Tamoxifen on Pituitary Gonadotropin Release In Vitro http://www.ncbi.nlm.nih.gov/pubmed/6781360
 
Also in this study, "Off-label use of SERMs, such as clomiphene citrate, are effective for maintaining testosterone production long-term and offer convenience of representing a safe, oral therapy. At present, routine use of aromatase inhibitors is not recommended based on a lack of long-term data."1 2

1Treatment of Hyopgonadotropic Male Hyopgonadism: Case-Based Scenarios - http://www.ncbi.nlm.nih.gov/pubmed/25949938
2 Effect of Rejuvenation Hormones on Spermatogenesis - http://www.ncbi.nlm.nih.gov/pubmed/23663992
 
Here is another study of pertaining to the question at hand.

"Tamoxifen, a selective estrogen receptor modulator (SERM), possesses central estrogen antagonistic effect but peripheral hepatic agonist effect, lowering IGF-1. Thus, tamoxifen is likely to perturb the neuroendocrine regulation of GH and gonadal axes." The study found that Tamoxifen, but not raloxifene, significantly reduced IGF-1 levels by 25+/-6% and increased SHBG levels by 20+/-7% at a therapeutic dose. Tamoxifen did, however, increase Testosterone (40%) and LH (70%) levels.1

Moral of this is that an increase in testosterone production is good, yes. However, an increase in testosterone production with an even more dramatic increase in SHBG actually could reduce free testosterone levels... which is important as this is what has the highest bioavailability (what your body can actually use). If more testosterone is bound to SHBG in the blood then it isn't binding to and activating the AR, which means the activated AR complex isn't translocating to the nucleus where it can influence gene transcription and protein synthesis. So, an increase in total testosterone may sound great, but unless they provided information on the levels of free testosterone in relation to total serum testosterone and showed a significant increase in free testosterone in response to the tamoxifen treatment despite the increase in SHBG, one must be left to assume that there was a negligible change, if not decrease, in the amount of usable (free) testosterone. Also of note, IGF-1 levels declined by 19-31%! This is a huge factor to consider. Insulin is THE MOST anabolic hormone known to man, of which IGF-1 (insulin like growth factor 1) shares a very similar molecular structure. Such a large reduction in IGF-1 levels are certainty not going to be beneficial to maintaining an anabolic state.

Too many people like to oversimplify how testosterone works in the body and automatically assume that more testosterone is better. As a matter of fact, this is most definitely not the case. The level of free testosterone is a very different thing than the level of bound testosterone and total serum testosterone. Other factors that must be taken into account are AR expression, protein content, mRNA etc. Even if all factors are perfectly accounted for, there's still the possibility that an induction of gene transcription isn't taking place.. fact of the matter is that without this induction, you won't see diddly squat happen on a macro level. Just because an increase exists in any one of these or even all of these doesn't necessarily mean that you're going to experience gains. In actuality, there is far more to how our bodies grow than what we currently understand - just to throw this whole thing on its head, there was a study where it was shown that testosterone isn't even necessary for muscle growth (I don't have the reference on hand but if I can find it I'll post that up for discussion).

1 Neuroendocrine Regulation of Growth Hormone and Androgen Axes by Selective Estrogen Receptor Modulators in Healthy Men - http://www.ncbi.nlm.nih.gov/pubmed/20843951
 
Too many people like to oversimplify how testosterone works in the body and automatically assume that more testosterone is better. As a matter of fact, this is most definitely not the case. The level of free testosterone is a very different thing than the level of bound testosterone and total serum testosterone. Other factors that must be taken into account are AR expression, protein content, mRNA etc. Even if all factors are perfectly accounted for, there's still the possibility that an induction of gene transcription isn't taking place.. fact of the matter is that without this induction, you won't see diddly squat happen on a macro level. Just because an increase exists in any one of these or even all of these doesn't necessarily mean that you're going to experience gains. In actuality, there is far more to how our bodies grow than what we currently understand - just to throw this whole thing on its head, there was a study where it was shown that testosterone isn't even necessary for muscle growth (I don't have the reference on hand but if I can find it I'll post that up for discussion).

Sorry to slightly hi-jack the thread, but I completely agree with this paragraph. MPS and mTOR signalling (among other pathways) isn't only stimulated by testosterone and/or AR-mediation, but by a whole variety of things from amino acids, medicinal pharms, nutritional supplements to the various growth hormones (MGF, insulin etc) and myostatin blockers. And of course we now know that many (perhaps all) AAS mediate some of their effect without interacting with the AR at all.

It's one reason getting bogged down in discussion of the 'perfect cycle' and the 'perfect steroid' - the often rather one-dimensional detail of AAS and their AR effect - as they do on most boards, is so myopic and uninteresting from my point of view. It's why we need to focus on the whole range of dietary, hormonal and supplement strategies when optimising for maximal muscle growth (ie the big picture).
 
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