Showing 1–12 of 147 results

Anabolic/Androgenic Steroids (AAS) are available in an oral form.  Orally administered AAS are very susceptible to first pass liver deactivation unless chemical molecular structures are altered to make them harder to deactivate. When an oral AAS is swallowed it enters the stomach where it is partially broken down and passed to the small intestines. The small intestines contain a group of enzymes called CYP-450’s. These enzymes begin to break down the AAS further in an attempt to deactivate it. The AAS is then absorbed through intestinal mucosa cells and transferred to the liver portal vein for further deactivation into inactive chemicals such as etiocholanone. These chemicals are then conjugated with glucuronic acid and excreted in urine. Up to 100% of the original compound can be deactivated in this process which is known as first pass deactivation.
By altering the steroid molecule structures deactivation can be greatly reduced. Some AAS are made orally active by adding an alkyl (methyl or ethyl) chemical group to the alfa position of the 17th carbon. These are commonly called c17 alfa-alkylated or methylated AAS. This creates a heavy load upon the liver and will alter or affect enzyme and other chemical levels. This is why orals, particularly methyltestosterone and Anapolon-50, might be harmful if administered for prolonged periods and in high dosages. The reason that this alteration is done is that more of the AAS enters the blood stream and remains active for a prolonged period. The reader should note that it is these c17 alfa-alkylated alterations that cause the possible liver dysfunction and not the original testosterone molecule. For this reason Andriol orals are reasonably liver friendly due to the fact that it is not altered in this way.