The best estrogen maintenance drug

Formestane is the first in a new line of selective, steroidal-based aromatase inhibitors. It is currently available in a few European countries, and is expected to reach U.S. shelves before long. Formestane is structurally a derivative of androstenedione, most specifically 4-OH androstenedione. Androstenedione is a readily aromatized steroid, so clearly this similarity welcomes interaction with the aromatase enzyme. Its activity in the body is in fact that of a suicide inhibitor, meaning that the compound will become inextricably bound to the aromatase enzyme upon contacting it. Its effect is therefore comparatively much more lasting than that seen with reversible, competitive inhibitors. This is no doubt the reason formestane was shown in studies to be as much as 60 times more potent than aminoglutethimide. As with Arimidex, this compound can help achieve near total suppression of aromatase.
Due to poor oral bioavailability, formestane is commercially prepared as an injectable product. The typical recommendation is an injection of 250mg (typically 1 ampule or injection) every two weeks. Though estrogen suppression can be marked with this dosing pattern, some studies do suggest that by the second week (near the time the dosage is to be repeated) estrogen levels may begin to recover.
The BEST estrogen maintenance drug?
Clearly there is more to consider in choosing an estrogen maintenance drug than just which is the most effective. The discussed differences in cholesterol alterations between anti-estrogens and aromatase inhibitors for example are worth taking into account. In this regard an antiestrogen such as tamoxifen or clomiphene would be most preferred. This is in great contrast to aminoglutethimide, Nolvadex or Clomid, which can cost $100 or less monthly. By measure of which is the most efficient remedy for estrogenic side effects, it would seem that Arimidex and formestane would technically be the most effective. Though more expensive, formestane was actually shown to be slightly less reliable than Arimidex in head to head studies, so its higher price should not automatically lead us into thinking it is the superior of the two. Ultimately however, it is doubtful that either of the new selective aromatase inhibitors (or other related agents slated to be released) will prove to be leagues ahead of the already tried and accepted estrogen maintenance drugs Nolvadex, Clomid and aminoglutethimide in the eyes of athletes. This is simply because the mentioned agents all deal with the action/buildup of estrogen quite effectively (in terms of clinical effectiveness of three agents compare closely to the new selective inhibitors), and outside of a medical setting the high cost of these newer agents will likely prohibit wide spread use.

Bodybuilding And Creatine

Creatine (methylguanidine-acetic acid) was discovered in 1832 by Michel Eugene Cheverul. Later on, in 1834 Justus von Lieburg “confirmed” that creatine was a normal part of meat. It was also found that there was more creatine in wild animals which underwent more exercise than animals that were living in captivity which exercised less.
During the early part of the 1900s by using creatine as a supplement allowed for a boost in creatine in animals. Later on, phosphocreatine (creatine phosphate or phosphorylated creatine) was discovered in the year of 1927. Then in 1934, the creatine kinase (the enzyme that “catalyzes” phosphocreatine was found). Finally, in 1968, phosphocreatine was found in the process of recuperating from exercise.
In foods, creatine is found primarily in red meat and fish. Eaten creatine is then eventually sent to the bloodstream. Creatine is also synthesized within the body by the liver, kidney and pancreas, although this primarily takes place in the liver. This is done in two steps: the first step is when an amidine group from arginine goes to glycine to make guanidinoacetic acid. Then in step two, a methyl group goes to a guanidinoacetic acid from S-adenoslymthionine forming creatine. In the synthesis of creatine, there are some controls on it so that when there is less creatine in one’s diet, there will be more synthesis of creatine in the body. In opposition, if there is a lot of creatine present in one’s diet, then there will be less creatine synthesis in the body.
The storage of creatine in the body occurs in two forms; in the form of phosphocreatine or simply creatine. In the average adult male weighing 70kg, there is 120g of creatine of which 95% is found in the skeletal muscle. Some of the creatine goes to other various parts of the body such as the heart and brain. Of all the creatine in the skeletal muscles, 60-70% of that creatine is phosphocreatine. And because it is phosphocreatine, it cannot leave the membranes.