If supplementing with 5mg daily whilst on cycle, when should one stop taking, after the last injection or at the end of PCT?
after last injection - if you are to stop at all.
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Should you not stop at all then?
why are you taking it?
prostate or hair?
for hair you should only need 1mg...
i've ditched the finsteride entirely
here is why
most strength athletes aren't touching finasteride
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Mainly for hair loss. I will be taking 320 mg saw palmetto for prostrate health
Is it better to take in liquid form or tablet, im trying to get the tabs off my source
I know that lowering the DHT levels will effect strength gains but id much rather have a full hair of head!!!
5mg is a lot.
1mg is 98% as effective as 5.
0.5mg is 90% as effective as 1mg and has 1/5 the reported sides.
I take 0.5mg year round and have no sides.
Since you wrote "last injection" I figure you have some long-lasting testosterone or steroid. Depending on how long-lasting it is, the finasteride is probably useful to take until that injection "wears off."
And also, KD1 is right about 1mg vs 5mg.
It might be a good idea to run it through PCT also if you are using an AI that boosts natural test.
as people post papers on related topics, I will do my first official copy and paste on AM.
This is related to using Finasterade for PRE-PCT.. interesting read. enjoy.
Pre-Post Cycle Therapy?
by Anthony Roberts
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)(Cool. 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.
1. Biol Reprod. 1985 Oct;33(3):603
2. Effect of inhibiting 5 alpha-reductase activity on the ability of testosterone to inhibit luteinizing hormone release in male sheep.
Biol Reprod. 1994 Jun;50(6):1244-50
3. Steroidal antiandrogens and 5alpha-reductase inhibitors.
Curr Med Chem. 2005;12(Cool:927-43.
4. Wilson JD 1996 Role of dihydrotestosterone in androgen action. Prostate 6(Suppl):88–922)
5. Russell DW, Wilson JD 1994 Steroid 5-reductase: two genes/two enzymes. Annu Rev Biochem 63:25–61
6. Thiboutot D, Harris G, Iles V, Cimis G, Gilliland K, Hagari S 1995 Activity of the type 1 5-reductase exhibits regional differences in isolated sebaceous glands and whole skin. J Invest Dermatol 105:209–214
7. Courchay G, Boyera N, Bernard BA, Mahe Y 1996 Messenger RNA expression of steroidogenesis enzyme subtypes in the human pilosebaceous unit. Skin Pharmacol 9:169–176
8. Sawaya ME, Price VH 1997 Different levels of 5-reductase type I and II, aromatase, and androgen receptor in hair follicles of women and men with androgenetic alopecia. J Invest Dermatol 109:296–300
9. Eur Urol. 1991;20 Suppl 1:78-81.
5 alpha-metabolism in finasteride-treated subjects and male pseudohermaphrodites with inherited 5 alpha-reductase deficiency. A review.
10. Human Anatomy and Physiology, 6th ed. John W. Hole jr. WCB Publishers.
11. Gormley GJ, Stoner E, Rittmaster RS, Gregg H, Thompson DL, Lasseter KC, Vlasses PH, Stein EA 1990 Effects of finasteride (MK-906), a 5-reductase inhibitor, on circulating androgens in male volunteers. J Clin Endocrinol Metab 70:1136–1141
12. J Clin Endocrinol Metab. 2005 Jul;90(7):4232-7. Epub 2005 Apr 5.Combined inhibition of types I and II 5 alpha-reductase selectively augments the basal (nonpulsatile) mode of testosterone secretion.
13. Neurobiol Aging. 1995 Jul-Aug;16(4):647-50.
14. J Clin Endocrinol Metab. 1994 Apr;78(4):916-21
i have heard over and over again that taking Deca and Finasteride results in more hair loss than taking just the deca (although i thought deca had nearly zero effect on hair loss)
that would suck as i would certainly take finasteride at .5mg/day on any test cycle and if it reacts badly with deca than that pretty much means i will never be using deca
is this true? what kind of logic/studies is this myth/truth rooted in? are there other AAS that finasteride should NOT be taken with?
I hear that it is a complete myth.Originally Posted by neverstop
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I heard a nandralone product would convert to DHN and finasteride protects against dht only so the DHN would attack the scalp. I also heard DHN is weaker than DHT. spiro is supposed to be used for a nandralone cycle.
I read that pre pct article and asked around here with no comments on it. so I'm interested in thoughts about it too.
Yeah, I'm going to do it at the end my current cycle.. It can't hurt.. I don't have MPB anyhoo.
would the issue with deca + fina be a concern with tren as well. I am looking at running .5 mg fina throughout cycle.
interesting read for sure.....thanks!