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Thread: Proviron what is it good for????

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    Proviron what is it good for????

    I ran across this post the other day and was quit surprised to read it. I have used proviron before between 50-100mg ED. I was sure it increased my libido. Although i have a hard time relying on my experiences cause there is just too many factors that go into if something is giving you an effect, so sometimes i sit back and ask myself was it really the proviron? or did my tren kick in and make me a horny dog? I have heard people say it reduces water, even that it decreases aroma. I just really wanted to share this opinion and see what you guys thought about it.

    from Dr. Scally

    This is a post on placed on another thread concerning the same topic.

    Dianabol (methandione, methandrostenolone, metandienone, and a host of other names) suppresses the HPTA. The use of dianabol in the hope that it will provide HPTA normalization is misguided. More details, later, can be provided, if requested.

    However, a brief note on proviron. What evidence is there that proviron lacks androgenic activity. The literature presents this by the absence of proviron to influence significantly infertility, erythropoiesis, lipids, and sex hormones. Except for the obsessive compulsive that needs to take a substance, thus replacing an AAS with adverse HPTA effects with one that does not, proviron is a worthless AAS, useful for nothing. Proviron will not support or provide any basis for the return of HPTA function.

    The quoted abstract from the study by Varma and Patel really does not give one any information. [Varma TR, Patel RH. The effect of mesterolone on sperm count, on serum follicle stimulating hormone, luteinizing hormone, plasma testosterone and outcome in idiopathic oligospermic men. Int J Gynaecol Obstet 1988;26:121-8.] The study is poor from the abstract alone. Please note that the statement, "Mesterolone had no depressing effect on low or normal serum FSH and LH levels but had depressing effect on 25% if the levels were elevated," refers unidentified group. The groups in the study include, "One hundred ten patients . . . had normal serum FSH, LH and plasma testosterone, 85 patients . . . had low serum FSH, LH and low plasma testosterone." Nowhere is there a group with elevated levels. Nonetheless, the cited effect is a "depressing effect" not stated as significant. Knowing the fluctuation in gonadotropin levels on testing even at a P<0.05 would not be meaningful. But it does go to the point that proviron has no adverse effect on the HPTA.

    Mesterolone is useless for infertility. A year after the Varma study, 1989, the World Health Organization published a study demonstrating, "[n]o significant changes semen quality during the course of the study, apart from an increase in sperm concentration 3 months after the start of treatment. The increase was greatest among the placebo treated group, but did not differ significantly between treatment groups." [Mesterolone and idiopathic male infertility: a double-blind study. World Health Organization Task Force on the Diagnosis and Treatment of Infertility. Int J Androl 1989;12:254-64.]

    In 1991, a study concludes, "Because similar semen improvement also occurred in the placebo controls, our findings cast doubt on the possible usefulness of high-dose Mesterolone treatment of idiopathic male infertility." [Gerris J, Comhaire F, Hellemans P, Peeters K, Schoonjans F. Placebo-controlled trial of high-dose Mesterolone treatment of idiopathic male infertility. Fertil Steril 1991;55:603-7.]

    These confirm an earlier study from 1983. [Wang C, Chan CW, Wong KK, Yeung KK. Comparison of the effectiveness of placebo, clomiphene citrate, mesterolone, pentoxifylline, and testosterone rebound therapy for the treatment of idiopathic oligospermia. Fertil Steril 1983;40:358-65.] Treatment with the mesterolone (100 mg/day) therapy did not result in a significant increase in the mean sperm concentration or pregnancy in the partners.

    Proviron is useless in promoting erythropoiesis (formation of red blood cell elements) and bone formation (a mixed effect of testosterone through the androgen receptor and estradiol receptor), both evidence of androgenic activity. Mesterolone (100 mg/d) is ineffective in raising hemoglobin and hematocrit levels significantly from baseline in individuals with hypogonadism. The study cites that Mesterolone did not increase serum testosterone (but also did not mention that there is a decrease). [Jockenhovel F, Vogel E, Reinhardt W, Reinwein D. Effects of various modes of androgen substitution therapy on erythropoiesis. Eur J Med Res 1997;2:293-8.]

    As recent as 2003, mesterolone (100 mg/d) for 6 months administered to hypogonadal males failed to significantly raise bone mineral density (BMD). Treatment with testosterone undecanoate (160 mg/d), testosterone enanthate 250 mg (every 21 days), or a single subcutaneous implantation of 1,200 mg crystalline testosterone did result in BMD increases. [Schubert M, Bullmann C, Minnemann T, Reiners C, Krone W, Jockenhovel F. Osteoporosis in male hypogonadism: responses to androgen substitution differ among men with primary and secondary hypogonadism. Horm Res 2003;60:21-8.]

    Erythropoiesis and bone formation are positive aspects of androgens useful under certain clinical conditions. AAS consistently have adverse effects on lipid profiles that are generally observed as a decrease in HDL (good cholesterol). In 1999, twenty years after the study cited by MaxRep [Nikkanen V. Plasma cholesterol, triglycerides, FSH and testosterone levels of normolipemic male patients with decreased fertility treated with mesterolone. Andrologia 1979;11:33-6.] proviron was found to adversely effect the lipid profile in hypogonadal men. The study by abstract analysis is hard to detail but an adverse effect of proviron is reported. Also, the study reports on serum testosterone levels with androgen treatments. Androgen substitution led to no significant increase of serum testosterone in the proviron group, subnormal testosterone in the testosterone undecanoate group, normal testosterone in the testosterone enanthate group, and high-normal testosterone in the crystalline testosterone group. The message is proviron did not affect the HPTA. [Jockenhovel F, Bullmann C, Schubert M, et al. Influence of various modes of androgen substitution on serum lipids and lipoproteins in hypogonadal men. Metabolism 1999;48:590-6.] The same author reports that proviron administration has no effect on serum FSH or testosterone. [Nikkanen V. The effects of mesterolone on the male accessory sex organs, on spermiogram, plasma testosterone and FSH. Andrologia 1978;10:299-306.]

    "I have said too much already. A further review of proviron literature will not change the use of proviron as an AAS for either anabolic or androgenic effects. Bottom line: Proviron is of no use for anything.

    Thank you."

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    Very super intense boners is all I found it good for. It's so intense. lol

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    Quote Originally Posted by Rastapopolous View Post
    Very super intense boners is all I found it good for. It's so intense. lol
    lol thats what i thought!!! but now im confused cause there is substantial evidence here that it has no androgenic effects, so was it really the proviron??? or was it due to decreased SHBG????

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    Quote Originally Posted by THE-DET-OAK View Post
    lol thats what i thought!!! but now im confused cause there is substantial evidence here that it has no androgenic effects, so was it really the proviron??? or was it due to decreased SHBG????
    AMEN.. i ran 100mg ED of this durring my cycle and stopped it around week 8 and noticed NO difference.. i still had to take an AI while i was on as well.. it is worthless.

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    Proviron is a DHT Derivative. DHT plays a major role in erections. Apparently it doesnt have much effect on the HPTA, but i wonder if it has a effect on the enzyme for conversion of test to dht.

    * Or those who have high conversion rates to DHT, take this while on cycle and it can act like fina/winny? (just the inhibition)

    basically what im kinda gettin is that u can take it during PCT to help with libido issues instead of viagra.

    but a depressing of 25% in elevated test patients? hmm... Wonder if it induced more conversion to DHT?
    Last edited by lemonada9; 05-10-2011 at 01:24 PM.

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    Quote Originally Posted by lemonada9 View Post
    Proviron is a DHT Derivative. DHT plays a major role in erections. Apparently it doesnt have much effect on the HPTA, but i wonder if it has a effect on the enzyme for conversion of test to dht.

    basically what im kinda gettin is that u can take it during PCT to help with libido issues instead of viagra.

    but a depressing of 25% in elevated test patients? hmm... Wonder if it induced more conversion to DHT?
    if it did produce more DHT conversion wouldn't that mean it would have increased BMD??? and about that suppression study, after that statement i think that study is worhtless. i mean it is suppressive on a normal funcitoning HPTA? but not on a partially suppressed?? what does that even mean? that pretty much tells me it IS suppressive not the opposite. i mean who cares if it didnt suppress a pratially suppressed HPTA, that does not mean it will not inhibit normalization? the guy even states it has a depressing effect, just not significant.............well ok then lol
    Last edited by THE-DET-OAK; 05-10-2011 at 01:42 PM.

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    no i was saying that it slows conversion to DHT due to more 'product'... *not sure BMD acronym*... but then there was no elevated test


    Lol. this is all a big mess... First google study found Mesterolone suppressive to test

    Effects of an androgenic-anabolic steroid on strength development and plasma testosterone levels in normal males

    The effects of an androgenic-anabolic steroid (mesterolone) on strength development, anthropometric measurements, body weight, aerobic power and pituitary-testicular function have been studied. A physically homogeneous group of 21 healthy males, aged 21-27, participated in an 8 week progressive weight training program during which 10 of the subjects received the steroid on a double-blind basis in doses of 75 and 150 mg/day respectively for the first and last 4 week period. All the subjects were given a 30 g supplemental-protein diet (including minerals and vitamins) daily. Although the steroid group showed gains over the controls in two of four maximal strength tests (isometric), the differences were not significant. No difference in body weight or aerobic power between the groups was observed. A significant increase over the controls in the circumference of the thigh was found. The steroid group revealed a significant suppression of the total plasma testosterone level, due to a reduction in the protein binding of testosterone in plasma. This suppression was most pronounced during the high dose (150 mg/day) drug administration period

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    lol i know huge mess, fvcking wasted my money lol. i ll just stick to masteron, unitl i find out its worhtless hahahaha

    BMD-bone mineral density, but now i know what you meant

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    I thought estrogen was the big factor in BMD?...

    but hea DHT is a regulator of estrogen...

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    In men, low T levels are usually come along with low BMD. Androgen therapy will increase BMD. So that was my point brudda.

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    yea wouldnt androgen therapy increase conversion of test to estrogen? increasing the estrogen, increasing BMD

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    I dont think that is why lem, deca and tren increase BMD as well.

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    It said the effects of Proviron are near to useless on cycle in the other thread, but now because you have managed to find an article by Michael Scally, you now believe its the truth.

    You seriously need to broaden your horizons and start reading other's opinions on AAS, not one HRT doctor.

    Proviron (Masterolone) exerts strong androgenic activity but weak anabolic action. How? Because, just like DHT, Masterolone is rapidly metabolised to weak diol metabolites in muscle tissue where concentrations of the 3-hydroxysteroid dehydrogenase enzyme's are high. That means its going to do next to nothing for muscle loss or LBM acurial.

    You'll get the positive androgenic effects (aggression, mood, labido, possibly strength, CNS) but thats where it ends.

    If you want to split hairs and argue it lowers SHBG on cycle, fair enough. But we both know what happens to SHBG on cycle in most cases.

    I wasted my money on this crap the first 2 cycles I conducted and ended up with a small case of gyno and terrible acne/scars.

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    why do you think i started diggin harder???? so i could get to the bottom of it, you are referring to the other thread, the reason why i was hammering SHBG is because of HIS specific situation. if it wasnt for our conversation, i would not have even thought about diggin harder.

    I am one of the most fair thinkers out there and am always open to new ideas, but until it can be proven im still skeptical, cause its really just anecdotal or pressumptions. Scally is the the best poster I have ever seen at backing up his arguments, because of his prior work history, he understand the behind the scenes bullshit in these studies, that why i quote him, he has no problem going against the grain.

    I appreciate you taking the time to respond. if you look closely at the other thread, i welcomed your opinion and was happy to hear it, until it became derragatory.
    Last edited by THE-DET-OAK; 05-10-2011 at 02:19 PM.

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    Deca and Tren are very similar to estrogen hence the similarity of sides (estrogen, deca + tren)

    if increasing test increased BMD, then wouldnt clomid/HCG/nolva all increase BMD? because they all raise test levels.

    Found it...


    It is interesting to note that estrogen is necessary for bone strength in men. This has been clearly demonstrated in men who lack aromatase, the enzyme which converts testosterone into estrogen. These men fail to close their epipheses and grow tall, but the bone density is low. Treatment with estrogen reverses the abnormalities.
    http://courses.washington.edu/bonephys/opmale.html#TEST


    makes a point although they are elderly studies

    http://www.annals.org/content/133/12/951.short
    Conclusions: In elderly men, hypogonadism related to aging has little influence on bone mineral density, but serum estradiol levels have a strong and positive association with bone mineral density.
    Last edited by lemonada9; 05-10-2011 at 02:21 PM.

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    lem you lost me buddy

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    Deca and Tren are similar compounds. they are estrene steroids which ultimately have similar effects as estrogen.
    There is some cross talk between the 'hormone response element' (basically after the binding, the transcription/lation ... etc) which affects which genes are transcribed. Thats how u can get some 'combined' results with modified sterols.

    very quickly put lol.

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    Quote Originally Posted by lemonada9 View Post
    Deca and Tren are very similar to estrogen hence the similarity of sides (estrogen, deca + tren)

    if increasing test increased BMD, then wouldnt clomid/HCG/nolva all increase BMD? because they all raise test levels.

    Found it...


    It is interesting to note that estrogen is necessary for bone strength in men. This has been clearly demonstrated in men who lack aromatase, the enzyme which converts testosterone into estrogen. These men fail to close their epipheses and grow tall, but the bone density is low. Treatment with estrogen reverses the abnormalities.
    http://courses.washington.edu/bonephys/opmale.html#TEST


    makes a point although they are elderly studies

    http://www.annals.org/content/133/12/951.short
    Conclusions: In elderly men, hypogonadism related to aging has little influence on bone mineral density, but serum estradiol levels have a strong and positive association with bone mineral density.
    This is exactly why I DO NOT suggest compounds that aromotase for those considered about epiphyseal growth plate closure.

    Estrogen is directly correlleted to BMD, thats exactly why SERMs increase BMD, Tamox, Tore (very good), Rolax, etc...

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    ^^ so would taking a AI during puberty make u taller?

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    Quote Originally Posted by THE-DET-OAK View Post
    why do you think i started diggin harder???? so i could get to the bottom of it, you are referring to the other thread, the reason why i was hammering SHBG is because of HIS specific situation. if it wasnt for our conversation, i would not have even thought about diggin harder.

    I am one of the most fair thinkers out there and am always open to new ideas, but until it can be proven im still skeptical, cause its really just anecdotal or pressumptions. Scally is the the best poster I have ever seen at backing up his arguments, because of his prior work history, he understand the behind the scenes bullshit in these studies, that why i quote him, he has no problem going against the grain.

    I appreciate you taking the time to respond. if you look closely at the other thread, i welcomed your opinion and was happy to hear it, until it became derragatory.
    Your not a "fair thinker" your arrogance has been pointed out by a number of senior members and staff here.

    Go and read others thoughts on AAS, not just Scally, trust me. He may be a sharp knife in the kitchen, but he's been wrong on some of his posts and those that know more have corrected him.

    Bill Roberts, Scally, Swale, William Llewellyn, Lyle McDonald, Alan Aragon and many more standard forum members (and those I have forgot) is where I learn, as well as various journals online.

    Not Michael Scally on his own...

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    Quote Originally Posted by lemonada9 View Post
    ^^ so would taking a AI during puberty make u taller?
    http://pediatrics.aappublications.or...21/4/e975.full

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    your being arrogant now, not realizing some of who you mentioned i talk to on the phone, regularly, and your arrogance was so high in the other thread you still fail to realize I was 100% correct about SHBG, for his particular situation, but you were so quick to pressume I did not know what I was talking about, you didnt even see the point i was try to make. .im out

    you sure make alot of pressumptions about me....................
    Last edited by THE-DET-OAK; 05-10-2011 at 03:28 PM.

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