Methyltestosterone

Methyltestosterone was developed synthetically in the search for an androgen that could be given orally, without loss of bioavailability. Mehyltestosterone is structurally similar to testosterone, except it is methylated at 17 position, which is associated with less hepatic metabolism following oral administration when compared to testosterone.

Methyltestosterone is an oral form of testosterone. Testosterone itself is ineffective when taken orally since the greatest part of the compound is metabolized and destroyed by the liver during the "first pass" so that at most 5-10% of the compound enters the blood and becomes effective. At a closer look methyltestosterone is a 17-alpha steroid molecule, which means that a methyl group is added to the C-17-alpha position of the molecule. Thus, methyltestosterone is not broken down and deactivated quite as fast by the liver as oral testosterone is. Still, it reaches the blood quickly and has only a low half-life time. Since methyltestosterone, in part, is reabsorbed through the mucous membrane in the mouth, this substance is also avail-able for sublingual intake. Methyltestosterone is a very potent ste-roid since it has a distinct androgenic effect. In particular, it is used to increase aggressiveness. Powerlifters and weightlifters use it be-fore a heavy workout or a competition since the increased andro-genic effect can already be noted one hour after intake and the improved aggressiveness, the increased self-esteem, and the thrust of motivation taking place allow the athlete to lift heavier weights. Those who try it will notice a quick and strong strength gain. The increase in body weight is within normal limits and is mostly due to water retention. The dosage is usually 25-50 mg/day. Methyltest is rarely taken if at all-for more than four weeks and women usually do not use it.

The action of Methyltestosterone is somewhat androgenic, with a moderate anabolic effect. As is typically seen with 17 alpha methylation, the resulting Methyltestosterone steroid has lower anabolic activity than its parent testosterone. Additionally it is extremely estrogenic, another property that seems to be enhanced when this alteration is present (when the steroid is receptive to the aromatase enzyme).

Methyltestosterone is used in the management of congenital or acquired hypogonadism. Methyltestosterone may be considered appropriate therapy for pathological, delayed puberty, and it is effective as palliative treatment for carcinoma of the breast in postmenopausal women, acting as an antiestrogen. Anabolic steroids have been the subject of drug misuse and abuse, often producing adverse effects such as changes in libido, hepatotoxicity, increased risk of cardiovascular disease, and antisocial behavior. Some of the masculinizing effects in women can be irreversible.

The function of androgens in male development begins in the fetus, is crucial during puberty, and continues to play an important role in the adult male. Women also secrete small amounts of androgen from the ovaries. The secretion of androgens from the adrenal cortex is insufficient to maintain male sexuality.

Normally, endogenous androgens stimulate RNA polymerase, increasing protein production. These proteins are responsible for normal male sexual development, including the growth and maturation of the prostate, seminal vesicle, penis, and scrotum. During puberty, androgens cause a sudden increase in growth and development of muscle, with a redistribution of body fat. Changes associated with endogenous androgens also take place in the larynx and vocal cords, deepening the voice. Puberty is completed with beard development and growth of body hair. Fusion of the epiphyses and termination of growth is governed by the androgens, as is the maintenance of spermatogenesis. Androgens have a high lipid solubility, enabling them to rapidly enter cells of target tissues. Increased androgen plasma levels suppress gonadotropin-releasing hormone, reducing endogenous testosterone, luteinizing hormone, and follicle-stimulating hormone through a negative-feedback mechanism. Exogenous replacement therapy stimulates the above process when endogenous supply is inadequate.