17-alpha-methyl-1-dehydroandrostanolone, or M1T for short, was the first methylated prosteroid introduced and initiated the “methyl craze” in the supplement market. No receptor binding studies have been performed on this molecule and the anabolic/androgenic ratios vary widely as well. Users have reported gaining 10 pounds or more in short periods of time (1-2 weeks). This compound cannot be converted to estrogen, is probably not appreciably progestational and is a DHT derivative. Side effects are those typical to androgens: acne, high blood pressure, altered lipids, prostate hypertrophy and male pattern baldness. It seems to be pretty potent and also seems to cause significant HPGA suppression. This compound is C-17 alpha alkylated so it does carry the risk of elevated liver enzymes, which should be similar or slightly more than equal doses of methandrostenolone. Methyl 1-test seems to cause lethargy in the same way as 1-test and reduces HDL levels quite severely. M1T was the most popular prosteroid until it was removed from the market with the passage of the 2004 Anabolic Steroid Control Act.
The likely mechanism for the rapid weight gain as well as the hypertension witnessed with M1T is an increase in water retention secondary to inhibition of 11-beta hydroxylase. Because M1T does not convert to estrogen, this water retention does not leak into the subcutaneous space resulting in the “bloated” look. The anabolic to androgenic ratios for this steroid range from weak to extremely potent. It is important to remember that water makes up 60-80 percent of the mass of muscle tissue. The water loading effect of some steroids will increase body weight quickly but transiently. This steroid has a reputation for being quite toxic but people still love it because it gives an instant gratification. Some have reported gynecomastia either while using M1T or post-cycle, often referred to as “delayed gyno”. As with oxymetholone, theories have been put forth to explain this effect including progestational effects and increases in prolactin. A more likely scenario, particularly for strong androgens with no conversion to estrogen, is that androgens reduce SHBG levels which can upset the androgen to estrogen ratio, particularly post-cycle when the androgenic stimulation of the cycle has subsided and back conversion of estrone to estradiol can upset the androgen/estrogen ratio. Another possibility is that inhibition of 11-beta hydroxylase will decrease cortisol levels but increase DHEA production by the adrenals. DHEA has been shown to be capable of directly stimulating the estrogen receptor.