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.]
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