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Old 06-02-18, 05:43 AM
A quantitative look at the multitudinous benefits of "Proviron" Mesterolone
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Lately I been seeing some chat across the forums about proviron, so lets brake this down and take a quantitative look at the multitudinous benefits of "Proviron" Mesterolone..

Here is some info in regards to proviron, it includes the benefit used with Test, tren, and assistance with low test levels and/or even depression....

What makes Priviron extremely beneficial in cycles/blast?

There's a few plausible explanations for this..

Proviron being a DHT in way it can/will lower SHBG levels which hinders estrogen formulation, thus providing the muscles with that "hard,dry appearance, less water retention"..Appearance so to speak, but there's more truth to this as I will explain below..

Proviron/mast work with a few different pathways, on the inside and outside of the AR's..Like mentioned in the initial post above, Proviron and Mast have been shown to increase the amount of free flowing test/bioavailability, greater blood plasma with Free test rather then bound, at the same time assisting test to stay in it's instructed pathways.. As you may know, Test has 3 functions.. 1)it's main course of action,being a main sex hormone/testosterone..2) Converting into estro, but lower SHBG hinders this in the presence of proviron..3) Test can convert into a MORE potent androgen such as DHT, and we know the functions of DHT as it tend to have a greater affinity for proteins over Test..

Testosterone alone has many functions that's often over looked when it concerns someone attempting to achive a harder, leaner look, in lieu people focus on other compounds when in fact Test in conjunction with proviron has a very pivotal role..

How does one achieve more definition,harder,leaner,more dry?
Now in the continuous supply of proviron or mast other AAS activities are almost amplified or undisturbed, allowing a great instance of protein synthesis..

(FYI; Androgen receptors are found throughout cellular groups, as well as FAT and muscle cell/groups, now we know that they initiate a response on AR's in muscle cells to promote size/growth, at the same given time they will have a cascade of effects on other cells and AR's found therein fat cells inducing activity/burning, thus the addition of proviron assist with AAS in these targeted tissue groups...Higher/more potent the androgen binds to the androgen receptors, the greater the lipolytic response will be on adipose tissue (brown or white)

Now lets also take into great consideration AR upregulation with the presence of androgens (more free flowing test), more AR sites throughout targeting tissue..,There's a vast amount of activity in which a complex interplay between activation and inactivation mechanisms and signaling between cell groups, what People need to remember that hormones are "chemical messengers" that rely messages to cells that display specific receptors for each hormone and respond to the signaling..Depending on the compounds and the individuals metabolization ratio the hormone can/may make changes directly to a cell, by changing the genes that are activated, or by making changes indirectly to a cell by stimulating other signaling pathways inside a specific cell group that is effected and effect other processes, thus this can "initiate" an intracellular cascade of events.. So, the notion that fat loss is NOT presence with proviron or mast, and to mitigate that AAS don't posses any fat loss properties is absurd...Should someone dial down their body fat to see greater results? This would be wise, but it's crucial..

IMO even a couch potato can see results with AAS, proviron, test, ext.. Now whether that lazy f*ck is deserving of it, that's a whole different topic!

So, in a nut shell.. Less presence of water retention, great affinity with protein vai muscle tissue, recovery, less estro related effects in specific targeting tissue, lower SHBG, more bio active test and presence from other androgens in or around AR's and other mediated tissue/muscle cells and other cellular groups and internal switches, improved pathways and other things etc etc etc..

Now mentions in the above abscracts about SHBG - SHBG is in fact the MASTER REGULATOR for Testosterone and Estrogen, having shifts within the static system and imbalances are often precipitated by SHBG abnormalities whether on or off AAS..

You don'there much mention about SHBG by come phtisicians while testing for T-serum level and I can explain why, That's because most don't even test for it, true story.. In fact most endo's go by the staple text book when it concerns therapeutic levels (by way of TRT)..But, we're not talking about therapeutic levels here, now when taking above theraputic levels there's enough evidence to support the importance of SHBG levels and the vital role of free test..

Free test is a VERY important number to monitor and maintain, as research has shown again and again, that free test is the one that actually works on skeletal tissue, in liue of a reserve bank..Total test matters without a doubt, because of the reserve that free test can built from..Bound Test to albumin may/can be bonded very loosely (depending in individuals ) and it will be ready to be available to do work when needed..

For those that may question the very importance of SHBG and suggesting SHBG means nothing while running Test, what about individuals that are prone to estrogen related sides? Higher SHBG may result in less active test, and more active estro in sensitive users..

Most endos only check for total test, that is all, unless a patient isn't reaching particular numbers within a range on a specific dosage, then they will order a panel for free test serum and SHBG looking for abnormalities..Keep in mind that even a great total test score can yield potentially false readings of what's actually taking place..Text book protocol can be very misleading.. For great reason I have such biased feelings towards Proviron..This read may summarizes on the pronounced properties of this underrated compound..

With this said lets discuss how it can assist with depression,aggression and/or anxiety,or other sides when on cycle/blast when utilizing Trenbolone, or at times other compounds and the same time "improving there performance/mechanisms..

Let's discuses Tren and one compound that can help assist with side effects that can be unbearable for most,especially anxiety..So lets talk about this shall we? There's more info added in regards to proviron being utilized with Test or other AAS, but the opening will cover the "Benefits while using Tren/Proviron combo"

Please allow me to illustrate one of the most shrouded and seldom discussed Drugs in the whole anabolic circuit, with one of the most underrated/pronounced effects ever, that somehow has failed to be discussed upon the masses...

"Proviron" Mesterolone (Masteron also applies as Proviron and mast can share the same pathways and expressions)

Most of you that have ever took the breakfast of champions "Methandrostenolone", That's right, I'm talking about Dbol. What's the most apparent and conspicuous effects that takes place while taking Dbol? If you were about to say the "sense of well-being" than your correct. One of the most profound and desirable effects that we can have during a cycle..Now, how about after a cycle? Or for longer duration's? But we all know that many of us practice moderation with harsh orals,or I would hope,But, have no concerns with elevated toxicity here!

One of the greatest characteristics about Proviron that has been shrouded and seldomly discussed is it's "Antidepressant" properties. With this being said, when it was first developed it was widely utilized in treatments for Bi-polar,OCD and Anxiety. As we know that depression is basically a chemical imbalance that comes about through the "Signaling" issues between receptors. Proviron improves the quality of the "channels" that the cells use to communicate and interact. Thus, a similar effect with Dbol where it drastically improves the sense of well being in users. Much like Antidepressants, SSRI (Selective serotonin re-uptake inhibitor, and/or,SNRI (Serotonin-nor-epinephrinere-uptake inhibitor)

What I'm about to share is a double blind study that clearly shows undoubtedly astonishing results in the patients! An other great reason to consider this compound.
Why proviron is underestimated, the world may never know

Tren is the compound that's well known for having a love hate relationship with most users. Most will deem it a necessary evil. But, in fact it doesn't have to be classified as evil after all..

Allow me to intro some clinical studies that have been conducted with a compound most commonly known as Proviron-trade name (Mesterolone).This agent posses some amazing characteristics with Antidepressant properties, as well Anti-anxiety.
It works by also metabolizing and being recognized through the endocrine as (other) a neurosteroid,effectively functioning as a so-called proneurosteroid (testosterone is also recognized as one).. These agents synthesized in the brain (Proviron especially) and have effects on brain function,In addition to their actions on neuronal membrane receptors,improving the quality of the channels that cells use to communicate and interact.

Proviron/or Masteron and Tren (Masteron can be utilized due to it's targeting similarities)
Proviron(mesterolone) will exert inhibitory actions on neurotransmission, acting as potent positive allosteric modulator of the GABA receptor (This is crucial concerning Tren-Insomnia as healthly function levels of GABA will produce a stable sleep state/environment for rest) and possess, in no particular order, antidepressant,stress-reducing, feeling warm/fuzzy/rewarding,pro-social, anti-aggressive(huge consider tren sides),pro-sexual,sedative/pro-sleep,cognitive-memory improvement..The list goes on!

(Where does this apply with Tren? It can aid all the way around with individuals how are sensitive or not.From the social aspect,overwhelming sense of anxiety,lack of sleep,basically everything stated above that may apply with the usage of tren and the onset of its unwanted side)

In addition to this information, an individual can also utilized masteron (Drostanolonein) in conjunction with Proviron, running both concurrent may yield a great synergenic effect,each compound will compliment one an other.

Below is a image illustrating the neurotransmitter/receptor and how it functions, also I will include some real actual studies conducted with proven results expressing the benefits of this compound (proviron)
Keep in mind that these doses may seem extreme,its been proven time and time again that such significant dosages are not needed to yield the effect. Merely a daily intake of 50-100 will suffice for almost anyone!

Further more Proviron is a DHT derivative. DHT compounds assist with hardening of the physique, lack of water retention,increased sex drive..Hardening of the physique and lack of water retention go hand in hand. Proviron assists with this, The body recognizes proviron as a DHT,This causes a direct hardening affect on the muscle tissue (Like mast posses,but mast is much more stronger IMO) The increase in hardness comes from a reduction in free estrogen levels, because proviron has the ability to 'latch-on' to the estrogen binding enzymes,It competes so to speak for its position,it does this aggressively, thus decreasing water retention. Also the the lack of aromatization and the fact that the drug is prototypical androgen, causes a significant shift in the body***8217;s estrogen/testosteroneratio.As proviron's atomic structure it is incapable of forming estrogen. It also has properties with AR's.. Increasing the AR expression, proviron/DHT uptake to further increase AR expression, repeating this process over and over ...
This allows other AAS compounds to appear to be amplified with there effects,assisting the compounds - (What does this mean?) It can be a master key so to speak, having multiple functions - It binds aggressively to the AR's and SHBG, thus it can/may increase the activity of other AAS/Androgens in the system) - This is an added bonus!

Functions concerning the neurotransmitter/receptor and how it works:Below is a image illustrating the neurotransmitter/receptor and how it functions, also I will include some real actual studies conducted with proven results expressing the benefits of this compound (proviron)
Keep in mind that these doses may seem extreme,its been proven time and time again that such significant dosages are not needed to yield the effect. Merely a daily intake of 50-100 will suffice for almost anyone!

Database: PsycINFO
[ Journal Article ]
A comparison of the antidepressant effects of a synthetic androgen (mesterolone) and amitriptyline in depressed men.
Vogel, William; Klaiber, Edward L.; Broverman, Donald M.
Journal of Clinical Psychiatry, Vol 46(1), Jan 1985, 6-8.


26 depressed male outpatients were randomly assigned to 14 wks of treatment with either mesterolone or amitriptyline in a double-blind parallel treatment design. Ss completed the Hamilton Rating Scale for Depression and a symptom checklist each week. Findings reveal that the drugs were equally effective in reducing depressive symptoms. Mesterolone produced significantly fewer adverse side effects than amitriptyline and did not produce hypomania or tachycardia, recognized side effects of amitriptyline. (10 ref) (PsycINFO Database Record (c) 2013 APA, all rights reserved)

Methods Find Exp Clin Pharmacol. 1984 Jun;6(6):331-7.
The effects of mesterolone, a male sex hormone in depressed patients (a double blind controlled study).
Itil TM, Michael ST, Shapiro DM, Itil KZ.
Based on computer EEG (CEEG) profiles, in high doses, antidepressant properties of mesterolone, a synthetic androgen, were predicted. In a double-blind placebo controlled study, the clinical effects of 300-450 mg daily mesterolone were investigated in 52 relatively young (age range 26-53 years, mean 42.7 years) male depressed outpatients. During 6 weeks of mesterolone treatment, there was a significant improvement of depressive symptomatology. However, since an improvement was also established during the placebo treatment, no statistically appreciable difference in the therapeutic effects of mesterolone was established compared to placebo. Mesterolone treatment significantly decreased both plasma testosterone and protein bound testosterone levels. Patients with high testosterone levels prior to treatment seem to have had more benefit from mesterolone treatment than patients with low testosterone levels. The degree of improvement weakly correlated to the decrease of testosterone levels during mesterolone treatment.

Information confirming no HTPA shutdown/suppression during PCT

These are some research articles that may justify the use of low/moderate dose Proviron during PCT:

AAKVAAG, A., and S. B. STROMME. "The effect of mesterolone administration to normal men on the pituitary-testicular function."Acta endocrinologica 77.2 (1974): 380-386.

Mesterolone (1***945;-methyl-5***945;-dihydrotestosterone) has been given to 10 normal men, age 24***8211;27 years, and the effect on the plasma levels of ICSH, FSH and testosterone has been studied.No effect on the plasma levels of ICSH and FSH could be detected. After 4 weeks on 75 mg mesterolone per day a significant (P < 0.01) drop in the mean value for plasma testosterone level was observed, 5.2 to 4.0 ng/ml. After another 4 weeks on 150 mg mesterolone per day a further decrease to 3.5 ng/ml was found.During mesterolone administration the protein binding of testosterone in plasma was significantly reduced, and it appeared that the level of free (non-protein bound) testosterone in diluted plasma remained unchanged, 0.37 and 0.41 ng/ml, before and after mesterolone administration respectively.The results suggest that mesterolone given in doses of 75 and 150 mg/day to normal men does not suppress the pituitary ICSH production or the testicular testosterone production

GORDON, R.D., THOMAS, M.J., POYNTING, J.M. and STOCKS, A.E. (1975), Effect of Mesterolone on Plasma L.H., F.S.H. and Testosterone. Andrologia, 7: 287***8211;296. doi: 10.1111/j.1439-0272.1975.tb00942.x

It has been claimed that orally administered mesterolone, unlike l7a-methyl testo- sterone, does not suppress endogenous gonadotrophins and testesterone. To investi- gate this, both drugs were administered, in turn, to four normal men and plasma te- stosterone, L.H. and F.S.H. were measured serially. Mesterolone administration was associated in all four subjects with significant and similar falls in plasma testosterone, but significant suppression of gonadotrophins took place in only two of them. Any changes which occured were apparent by the end of the first week of therapy. Administration of half the dose of 17a-methyl testosterone to the same four subjects caused significant suppression of testosterone in each and suppression of one or both gonadotrophins in each.
In longer term studies in patients (5-30 months) involving serial measurements at intervals of one to two months, there was evidence of significant suppression of L.H. and F.S.H. by 17a-methyl testosterone, but not by mesterolone, which was clinically a less effective androgen.

WANG, C., BURGER, H.G., de KRETSER, D.M., DULMANIS, A., HUDSON, B., KEOGH, E.J. and SUTHERS, M.B. (1974), Effect of Mesterolone on Serum FSH, LH and Plasma Testosterone in Normal Men. Andrologia, 6: 111***8211;117. doi: 10.1111/j.1439-0272.1974.tb01604.x

To determine whether the claim that mesterolone, an orally active androgen, does not cause suppression of gonadotrophin secretion, two groups of five normal men were treated with 100 and 200 mg. daily respectively for 7 days. Serial measurements of serum FSH, LH and plasma testosterone were made on samples taken at 15 minute intervals over 2 hr both before and during treatment. Modest falls in FSH, LH and testosterone levels were observed in both groups, the percentage suppression being 21% and 18% for FSH, 19% and 15% for LH and 9% and 8% for testosterone at the lower and higher dosage levels respectively.

200mg is a far greater dose than I would deploy during PCT (50mgs is ideal). From these studies and other articles we see have read, it's clear that there is almost minimal/no influence on the HTPA, any effect would be absolute minimal and negated by other appropriate compounds used during that period (HCG, Aromasin, Nolvadex and HGH)...



I'd also like to add some stellar information about "provirion" and its amazing proprieties..

Provirion won't suppress LH or FSH and will even provide your body with more free testosterone due to the fact that it binds "AGGRESSIVELY" to SHBG (lowering levels)....With this said it's not suppressive like most steroids, and your FREE T can greatly increase by allowing bound test to act in its original course of lieu of being bound (freeing up bound test)

Proviron will assist in a blast/cycle
It's already known that only a very small amount of Testosterone exists as free testosterone. Free test is testosterone that capable of binding to the Androgen Receptor, which is where all the rest of the magic happens, and allows for the following benefits:
-Enhanced growth factor activity (e.g. GH, IGF-1, etc.)
-Enhanced activation of myogenic stem cells (i.e. satellite cells)
-Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)
-Enhanced protein synthesis
-New myofiber formation

Testosterone binds at around 45% to what is known as Sex Hormone Binding Globulin (SHBG), and about another 53% binds to proteins (albumin). The rest exists in a free state (about 2% if you did your math). Different variations of steroids also differ in the way in which they bind to proteins.
If one could unbind testosterone from SHBG by even a small percentage, it could make a big difference in the way that testosterone or other AAS exert their anabolic effects. Studies show that when testosterone is unbound from SHBG the free test does in fact exert greater effects than total T. As the following studies support:
Demisch K, and Nickelsen T. Distribution of testosterone in plasma proteins during replacement therapy with testosterone enanthatein patients suffering from hypogonadism Andrologia 1983;15 Spec No:536-41.

Gandar R. Interpretation of the blood level of a steroid Rev Fr Gynecol Obstet 1985 Aug-Sep;80(8-9):635-40.

Legrand E., et al. Osteoporosis in men: a potential role for the sex hormone binding globulin Bone 2001 Jul;29(1):90-5.

Longcope C., et al. Diet and sex hormone-binding globulin. J Clin Endocrinol Metab 2000 Jan;85(1):293-296.

Valero-Politi J, and Fuentes-Arderiu X. Within- and between-subject biological variations of follitropin, lutropin, testosterone, and sex-hormone-binding globulin in men. Clin Chem 1993 Aug;39(8):1723-1725.

Proviron(1-Methyl Dihydrotestosterone) has been shown to bind with SHBG much more readily than test.

Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.

Saartok T, Dahlberg E, Gustafsson JA.

It is unclear whether anabolic steroids act on skeletal muscle via the androgen receptor (AR) in this tissue, or whether there is a separate anabolic receptor. When several anabolic steroids were tested as competitors for the binding of [3H]methyltrienolone (MT; 17 beta-hydroxy-17 alpha-methyl-4,9,11-estratrien-3-one) to the AR in rat and rabbit skeletal muscle and rat prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone ) greater than methenolone (17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one) greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05):stanozolol(17 alpha-methyl-5 alpha- androstano [3,2-c]pyrazol-17 beta-ol), methanedienone (17 beta-hydroxy-17 alpha-methyl-1,4-androstadien-3-one), and fluoxymesterolone (9 alpha-fluoro-11 beta-hydroxy-17 alpha-methyl-T). Other compounds had RBAs too low to be determined (e.g. oxymetholone (17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one) and ethylestrenol (17 alpha-ethyl-4- estren -17 beta-ol). The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction of its 3-keto function to metabolites, which did not bind to the AR [5 alpha-androstane-3 alpha, 17 beta-diol and its 3 beta-isomer (3 alpha- and 3 beta-adiol, respectively)]. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA in rat muscle to that in the prostate (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Skalba P, Korfanty A, Mroczka W, Wojtowicz M. Related Articles
[Changes of SHBG concentrations in postmenopausal women]
Ginekol Pol. 2001 Dec;72(12A):1388-92. Polish.

Variations of sex hormone-binding globulin in thyroid dysfunction.

Brenta G, Schnitman M, Gurfinkiel M, Damilano S, Pierini A, Sinay I, Pisarev MA.

Department of Endocrinology and Metabolism, French Hospital, Buenos Aires,

With the aim of understanding the variations of the levels of sex hormone-binding globulin (SHBG) in thyroid dysfunction, we studied the influence of factors that also modify SHBG, such as menopausal status, age, and body mass index (BMI) in women with hypothyroidism and hyperthyroidism, both overt and subclinical. Statistical analysis was performed by means of analysis of variance (ANOVA), stepwise multiple regression, and partial correlation. The ANOVA showed a significant statistical difference among the means of SHBG of all groups (p<0.01). The difference was due to the group that included hyperthyroid women. Multiple regression analysis showed that the main factors influencing SHBG were BMI and age, except for the hyperthyroid group, where the most important independent variables were triiodothyronine (T3) and thyroxine (T4). Partial correlation controlling the effect of BMI and age showed no association between SHBG and the other variables in all groups except for the subclinical hyperthyroid and hyperthyroid, where we found a significant association between SHBG and T4 and T3. The premenopausal or postmenopausal status did not modify SHBG levels. When the patients are taken as a whole, BMI, age, T4, and T3 all have an association with SHBG levels according to the multiple regression analysis.

Determinants of sex hormone-binding globulin blood concentrations in premenopausal and postmenopausal women with different estrogen status. Virgilio-Menopause-Health Group.

Pasquali R, Vicennati V, Bertazzo D, Casimirri F, Pascal G, Tortelli O, Labate AM.

Department of Internal Medicine and Gastroenterology, University of Bologna, Italy

Just a quote: 2) SHBG values are correlated positively with estradiol and negatively withinsulin and testosterone concentrations, but the predictive value of these variabiles on SHBG appears to be different in premenopause and postmenopause;

Here is a fun little fact: the level of SHBG can also be influenced by other factors. There is a direct relationship between the level of estrogen and thyroid hormones and the level of SHBG. Estrogen goes up, SHBG goes up. Estrogen goes down SHBG goes down. Same for Thyroid hormones triiodothyronine (T3) and thyroxine (T4). Also, there is a relationship with diet and insulin, but that is something I will save for later. Higher androgen levels due to AS administration has been shown to considerably lower levels of SHBG as well. The ASWinstrol (stanozolol) was shown in a 1989 study to lower levels of SHBG by 50% after oral administration.

Sex hormone-binding globulin response to the anabolic steroid stanozolol: evidence for its suitability as a biological androgen sensitivity test.

Sinnecker G, Kohler S.

Department of Pediatrics, University of Hamburg, West Germany.

Both the androgen-induced decline in serum sex hormone-binding globulin (SHBG) levels during puberty and the anabolic effect of exogenous testosterone are absent in patients with androgen insensitivity (testicular feminization). To determine whether the androgen-induced decline in serum SHBG could be used as a test of androgen sensitivity, we studied the effect of the anabolic-androgenic steroid stanozolol (17 beta-hydroxy-17 alpha-methyl-5 alpha-androstano-[3,2-c]pyrazol) on serum SHBG in 25 control subjects, 3 patients with complete androgen insensitivity, and 4 patients with partial androgen insensitivity. Stanozolol was administered orally for 3 days (0.2 mg/; blood samples were taken before and 5, 6, 7, and 8 days after the beginning of the test for measurements of serum SHBG. The lowest value (i.e. the peak response) in each subject was used as the measure of the response to stanozolol. In the control subjects the mean nadir serum SHBG level was 51.6 +/- 5.9% (+/- SD) of the initial value (P less than 0.001). In the 4 patients with partial androgen insensitivity the nadir serum SHBG ranged from 73-89%, and in the 3 patients with complete androgen insensitivity it ranged from 93-97% of the initial value. Thus, the decrease in serum SHBG after short term administration of stanozolol reflects androgen responsiveness and, thus, may be used to differentiate patients with androgen insensitivity syndromes from those with other causes of male pseudohermaphroditism.

Proviron could provide the mechanisms to increase the value of other AS... Proviron would work because by binding to SHBG, it leaves hormone in a free state to bind to the AR. Proviron is a terrible Anabolic, but its affinity for SHBG would essentially displace other steroids from binding to SHBG...Provirion would work to reduce the overall amount of SHBG, thereby having the effect of freeing up hormone to bind to the AR.
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