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Pre-Post Cycle Therapy?

April 10th, 2009 · No Comments

By now, most anabolic steroid users know that after a cycle, the use of certain compounds like SERMs (Selective Estrogen Receptor Modulators) and such speed recovery of the HPTA (Hypothalamic-Pituitary-Testicular-Axis). Less well known is how to integrate other compounds with SERMs for maximum recovery of the HPTA. Human Chorionic Gonadatropin, an Aromatase Inhibitor, and even nutritional supplements such as Vitamin E can all be used to create an environment conducive to maximum recovery after a cycle. In the world of anabolic performance enhancement, all of this comes together to be known as “Post Cycle Therapy” or PCT for short.

But, until this point, we have not known of many avenues for initiating recovery of one’s HPTA while still on-cycle. Let’s turn now to the science behind “Pre-Post Cycle Therapy” (pPCT) and how utilizing it can be of benefit to AAS users.

First, I’ll go through a bit of the Physiology (just some painless explanations of the major players, I promise) involved in the production of endogenous testosterone, as relates to what we’re trying to accomplish with…err…pPCT.

Testosterone is the primary male sex hormone. Testosterone is manufactured in the Leydigs cells in the testes, at about 2.5-11mgs/day for the average male, and is largely influenced by another hormone: LH (Leutenizing Hormone). LH promotes the secretion of testosterone by being released in pulses which trigger pulses of testosterone. For the purpose of pPCT, we’re hoping to bring LH secretion back online a bit before we completely stop our cycle. Both LH as well as testosterone are secreted in pulses between eight and fourteen times, daily. Testosterone secretion typically precedes an LH pulse by approximately one hour.

Testosterone is, of course, controlled via a negative feedback loop. As such, a higher level of testosterone in your body causes a decrease in LH, which in turn causes less testosterone to be released (10). Testosterone converts to Dihydrotestosterone (DHT) (4) in your body via the 5alpha-Reductase enzyme (5a-R). DHT is very odd from a biological point of view (or from mine, anyway)—more in a second. Testosterone also converts to estrogen via the aromatase enzyme.

DHT is considered quite androgenic compared to testosterone but is not highly anabolic because it is not very active in skeletal muscle (it is enzymatically deactivated by 3-alphahydrosysteroid hydrogenase). However, in most of the body, its androgenic effects are felt quite profoundly: in the brain (the CNS), skin and genitals DHT is the most active androgen because 5-AR is concentrated heavily in practically every androgen-dependent area of the body, barring skeletal muscle. Remember however that 5a-R is not DHT; we need to add testosterone to 5a-R to make DHT.

Now, let’s talk about DHT and 5-alpha-reductase, in terms of LH and testosterone. Dihydrotestosterone was shown to inhibit LH and FSH secretion and serum testosterone concentrations in male rams (1). In addition, and very importantly for this discussion, the actual conversion process of testosterone being metabolized into DHT via this 5a-R enzyme may act in some way to inhibit Leutenizing Hormone Release (2) (and ergo would inhibit your HPTA and natural testosterone production). Yeah, the actual conversion process is inhibitory.

Wouldn’t it be great if we could maybe use some steroids, and still take (at least) this one mechanism of inhibition away? Then perhaps some LH function would return, even before we ended our cycle….

Well, maybe we can, but let’s not get ahead of ourselves.

Basically, the following chart shows the baseline level of LH in male sheep given a 5-Alpha-Reductase inhibitor (Finasteride), then a chart showing the LH levels in sheep given testosterone propionate, and finally a chart showing LH levels of sheep given testosterone propionate + the inhibitor (graph 3 in the series)(2). You’ll note that although using the inhibitor alone produced no remarkable effects on LH at all, when administered with testosterone, it seems to have allowed LH pulsality to continue very much unaffected (slightly affected, but still very close to baseline) even though exogenous testosterone propionate was administered! Here’s that series of charts (all three are from reference 2):

Okay, so what are the implications here for AAS-using bodybuilders? Let me preface this by saying that I know we can not simply look at animal studies and extrapolate whatever conclusions we want from them. However, in this particular case, I feel that by keeping the conclusions conservative (yet still very much avant-garde), we won’t be disappointed nor will we be underestimating the value of this evidence. So, let’s look at Finasteride a bit more closely.

Interestingly, Finasteride only acts on the type II substrate of the 5a-reductase enzyme, and that may be important in examining why it inhibits suppression. The enzyme 5-reductase is present throughout the body in two forms, type 1 and type 2 (5). Type 1 is located predominantly in the skin, both in hair follicles and sebaceous glands, as well as in the liver, prostate, and kidney (6)(7)(8). Type II is found in the brain (where the pituitary is located, which is where LH is secreted), the prostate and male genitalia (where testosterone is released). It is also known that deficiency of the type II isoenzyme elevates both LH and Te concentrations, while suppressing type-I & II releases testosterone and LH in a nonpulsatile manner, which is problematic with LH/Testosterone, since it doesn’t mimic the natural secretion pattern (this is speculated in some studies to be why some GH protocols are, in the long run, less effective when the natural rhythm of secretion is not mimicked).

Finasteride, although it primarily acts on the type II substrate, was found to be a potent inhibitor of C19 androgen and C21 5 alpha-steroid metabolism, as well as both hepatic and peripheral 5 alpha-metabolism. What this means is that there are pretty specific 5-a Metabolic changes (i.e. the changes and metabolites produced by 5a-reductase) going on here, that seem to show a consistent decrease of both Dihydrotestosterone and 3 alpha-androstanediol glucuronide (both are markers of 5a-metabolism). This decrease is systemic, meaning it occurs everywhere that the conversion occurs. Some other stuff, like urinary C19 and C21 5 beta to 5 alpha steroid metabolite ratios also increase during Finasteride treatment, again meaning there is clearly less of this 5a- conversion.

The data I’ve reviewed also suggests that a 5 alpha-reductase gene codes for an enzyme with affinity for multiple steroid substrates (9), and of course, this may add to inhibition during the process we’re examining. All of these actions at the cellular (and possibly genetic) level that inhibit the conversion of testosterone into DHT contribute to why Finasteride happens to keep one’s LH levels from plummeting, even in the presence of exogenous testosterone. In fact, analysis of 10-min plasma LH sampling during either a 10-h or 24-h period demonstrated that the subjects with 5 alpha RD type-II substrate deficiency had a mean plasma LH level, mean LH pulse amplitude, and mean plasma LH nadir that were approximately twice normal (14).

Given all of this evidence, reducing one’s type-II 5a-R enzyme and the conversion it causes will more likely than not restore LH quite a bit, since at least part of the inhibition of endogenous LH (and corresponding testosterone levels) must occur via conversion in that first area I spoke of (the Brain, specifically, which is where your pituitary is located). This conversion process can be inhibited with Finasteride (13), and this is probably why the pulsatile secretion pattern seems to not face total inhibition even when exogenous testosterone is administered (2), as LH is now more free to be released (which we know leads to testosterone secretion).

We have identified the 5-a-reductase induced metabolism of testosterone into DHT as being inhibitory on LH pulses (which we know to originate from the pituitary). We also know that Finasteride specifically slows this conversion process in such a way as to allow a natural secretion pattern of LH to continue, albeit not at 100% (hey, nobody’s perfect), as other inhibitory factors will still be at work (remember, this isn’t PCT, it’s prePCT).

So how could we use this information to our advantage, to get a jump start on our PCT?

Okay, so let’s just say that one’s on a 16-week cycle (I’ll use a common one–Equipoise and Testosterone Propionate), and one’s 25 days from ending it. Well, I will speculate that one can (ideally) switch over to just the propionate (at around 100mgs, every 2nd day (EOD, in common parlance), which would give us a continued anabolic effect, yet would still fall shy of the 3 days of constant infusion of Testosterone Propionate utilized by the lab for the study in the chart (2). We’ll need to stay for about 10 days at this dose, to allow at least a minimal amount of clearance from the other compound(s) we’ve been using (in this case Equipoise).

The blood plasma levels of the other compounds, I would think, need to fall a bit, so by the time we begin the Finasteride treatment one will be primarily dealing with a reasonable dose of testosterone propionate, and not multiple compounds. This will both allow one to primarily deal with inhibition caused by the testosterone propionate, and also keep one from having to use the same whopping dose of Finasteride used in that same study (10x the amount necessary to inhibit 5a-Reduction of testosterone to DHT).

One will then begin administration of 2mgs/day of Finasteride. I know that the generally accepted dose for bodybuilders is only 1mg/day, but what we’re looking for here is a higher dose, although not as high as the dose that was previously used for treatment of prostate hyperplasia (the dose used in Proscar, not Propecia), as this would more closely mimic the amount used by the scientists in the study (2) relative to the amount of testosterone propionate we’d be using. This should result in a rise in LH pulses, and a concomitant rise in endogenous testosterone. Again, this certainly will not get us back to baseline alone, but will definitely give us a starting point far beyond what would be experienced if we were to simply run PCT with nothing before.

This is one way to begin the transition from the end of one’s cycle (pPCT) to your Post Cycle Therapy. Can you do it other ways? Sure. You can probably just run 1-2mgs of Finasteride for the last month of your cycle, and continue your regular doses of whatever compounds you’re running and still see a good jumpstart to your PCT.

Let me emphasize, that I’m not trying to say “use Finasteride on your cycles and you don’t need PCT” or “Finasteride will prevent any inhibition of HPTA.” My contention is much more conservative. After looking at the research, I am confident in proposing the use of Finasteride as a pre-Post Cycle Therapy agent that will make recovery during PCT faster and more efficient.

Tags: Anabolic Steroids · General · Steroids Cycles

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