The benefits of adding Proviron or Masteron to your Trenbolone Cycle
Posted: Thu Jul 23, 2020 12:03 pm
***This entire write-up including all research and citations is the work of PSL Supervisor and Head Representative Vision. I am simply sharing his work.
OR 
+ 
So, the discussion has came about many times over in regards to depression, insomnia, aggression, anxiety or other sides when on cycle/blast when utilizing Trenbolone..
Let's discuses Trenbolone and one compound that can help assist with side effects that can be unbearable for most, especially anxiety while using Trenbolone..
Please allow me to illustrate one of the most shrouded and seldomly discussed drugs in the whole anabolic circuit, one of the most underrated/pronounced effects ever
that somehow has failed to be discussed upon the masses, or misunderstood at best...Proviron!
"Proviron" Mesterolone
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 like during PCT, Or for longer cycle/blast duration's when we feel fatigued?
One of the greatest characteristics about Proviron 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" between receptors.
Proviron improves the quality of the "channels" that the cells use to communicate and interact, chitter chatter so to speak. 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.
Here I will introduce some clinical studies that have been conducted with a compound most commonly known as Proviron-trade name (Mesterolone).
This agent possesses 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 steroids synthesized in the brain much like a Nootropic (Proviron especially) and have effects on brains 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 (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 healthy function levels of GABA will produce a stable sleep state/environment for rest
and displays 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 literally goes on!
Where does this apply with Tren?
It can assist all the way around with individuals who are sensitive or not with trenbolone.
From the social aspect, overwhelming sense of anxiety, lack of sleep, basically everything stated above that may apply with the usage of trenbolone and the onset of its unwanted side..
In addition to this information an individual can also utilized masteron (Drostanolonein) in conjunction with Proviron (subsituting one for the other), running both concurrently may yield a great synergenic effect, each compound will compliment one an other.
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 much like Masteron displays..
The increase in muscle dryness/density comes from a reduction in free/circulating 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’s estrogen/testosterone ratio.
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"?
Proviron 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..
________________________________________________
Functions concerning the neurotransmitter/receptor and how it works:
Citation
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.
Abstract
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.
Abstract
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 endocrinologica77.2 (1974): 380-386.
ABSTRACT
Mesterolone (1α-methyl-5α-dihydrotestosterone) has been given to 10 normal men, age 24–27 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
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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: 287–296. doi: 10.1111/j.1439-0272.1975.tb00942.x
Summary
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.
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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: 111–117. doi: 10.1111/j.1439-0272.1974.tb01604.x
Summary
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.
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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)...
Team PSL supervisor
Vision
__________________________
Just an addition to the above read!
also....
Proviron will NOT 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, your total test probably may not increase much, however that's not what's important, your Free-T is the ticket..
Your FREE T will INCREASE 5-10 FOLD.. Its freed from bound test ultimately allowing test to act in its original course of action, in lieu of being bound!
If you're experiencing excessive sweating at night from Trenbolone you may want to consider limiting yourcarbs in the evening,
this tends to help because the body is in a state of thermogenesis so there's a slew of activity taking place, Its known as "thermoregulation" as an integral part of sleep homeostasis...
Your body will warm itself up, however during thermgenesis from powerful andros like tren, carbs fuel this process 10 fold...
Limit your carbs and my prove to be effective..
Last but not least, here's some more information that can provide you with achieving an environment that will assist with more FREE-T..
"Proviron with Winstrol"
Here's a study on proviron and winny together.
How winny and proviron will make your cycle kick ass!
Really, 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, Argentina. [email protected]
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 with insulin 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 AaS Winstrol (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/kg.day); 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.
__________________
Take away notes:
This was after oral administration, so I am not sure that I can extrapolate the data to injectable as well.
SHBG is made in the liver so even an injectable winny would have to be processed there, albeit slower, due to the slower release of injectable winny and it’s direct release into the bloodstream. That could possibly make it a little less effective in this regard.
In a nutshell: Proviron and Winny 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.
Winstrol would work to reduce the overall amount of SHBG, thereby having the effect of freeing up hormone to bind to the AR. What a stack!
I hope you enjoyed the read....
Team PuritySourceLabs,
Vision
OR + So, the discussion has came about many times over in regards to depression, insomnia, aggression, anxiety or other sides when on cycle/blast when utilizing Trenbolone..
Let's discuses Trenbolone and one compound that can help assist with side effects that can be unbearable for most, especially anxiety while using Trenbolone..
Please allow me to illustrate one of the most shrouded and seldomly discussed drugs in the whole anabolic circuit, one of the most underrated/pronounced effects ever
that somehow has failed to be discussed upon the masses, or misunderstood at best...Proviron!
"Proviron" Mesterolone
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 like during PCT, Or for longer cycle/blast duration's when we feel fatigued?
One of the greatest characteristics about Proviron 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" between receptors.
Proviron improves the quality of the "channels" that the cells use to communicate and interact, chitter chatter so to speak. 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.
Here I will introduce some clinical studies that have been conducted with a compound most commonly known as Proviron-trade name (Mesterolone).
This agent possesses 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 steroids synthesized in the brain much like a Nootropic (Proviron especially) and have effects on brains 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 (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 healthy function levels of GABA will produce a stable sleep state/environment for rest
and displays 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 literally goes on!
Where does this apply with Tren?
It can assist all the way around with individuals who are sensitive or not with trenbolone.
From the social aspect, overwhelming sense of anxiety, lack of sleep, basically everything stated above that may apply with the usage of trenbolone and the onset of its unwanted side..
In addition to this information an individual can also utilized masteron (Drostanolonein) in conjunction with Proviron (subsituting one for the other), running both concurrently may yield a great synergenic effect, each compound will compliment one an other.
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 much like Masteron displays..
The increase in muscle dryness/density comes from a reduction in free/circulating 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’s estrogen/testosterone ratio.
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"?
Proviron 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..
________________________________________________
Functions concerning the neurotransmitter/receptor and how it works:
Citation
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.
Abstract
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.
Abstract
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 endocrinologica77.2 (1974): 380-386.
ABSTRACT
Mesterolone (1α-methyl-5α-dihydrotestosterone) has been given to 10 normal men, age 24–27 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: 287–296. doi: 10.1111/j.1439-0272.1975.tb00942.x
Summary
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.
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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: 111–117. doi: 10.1111/j.1439-0272.1974.tb01604.x
Summary
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.
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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)...
Team PSL supervisor
Vision
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Just an addition to the above read!
also....
Proviron will NOT 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, your total test probably may not increase much, however that's not what's important, your Free-T is the ticket..
Your FREE T will INCREASE 5-10 FOLD.. Its freed from bound test ultimately allowing test to act in its original course of action, in lieu of being bound!
If you're experiencing excessive sweating at night from Trenbolone you may want to consider limiting yourcarbs in the evening,
this tends to help because the body is in a state of thermogenesis so there's a slew of activity taking place, Its known as "thermoregulation" as an integral part of sleep homeostasis...
Your body will warm itself up, however during thermgenesis from powerful andros like tren, carbs fuel this process 10 fold...
Limit your carbs and my prove to be effective..
Last but not least, here's some more information that can provide you with achieving an environment that will assist with more FREE-T..
"Proviron with Winstrol"
Here's a study on proviron and winny together.
How winny and proviron will make your cycle kick ass!
Really, 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:
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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, Argentina. [email protected]
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 with insulin 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 AaS Winstrol (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/kg.day); 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.
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Take away notes:
This was after oral administration, so I am not sure that I can extrapolate the data to injectable as well.
SHBG is made in the liver so even an injectable winny would have to be processed there, albeit slower, due to the slower release of injectable winny and it’s direct release into the bloodstream. That could possibly make it a little less effective in this regard.
In a nutshell: Proviron and Winny 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.
Winstrol would work to reduce the overall amount of SHBG, thereby having the effect of freeing up hormone to bind to the AR. What a stack!
I hope you enjoyed the read....
Team PuritySourceLabs,
Vision
