In the June 2015 issue of Applied Metabolics, I discussed new research that suggests dihydrotestosterone (DHT) may be the true cause of some controversial side effects related to testosterone therapy. DHT is a metabolic by-product of testosterone (T) produced by the conversion of T into DHT through the actions of enzymes called 5-alpha reductase (5AR). There are three versions of this enzyme, with the type-1 version being most active in the sebaceous glands of the skin and in the liver. The increased activity of type-1, 5-alpha reductase enzyme in the skin's sebaceous glands promotes an increased secretion of oil in the skin, which is also related to the increased incidence of acne. The high incidence of acne often seen in those who use anabolic steroid drugs is caused by certain steroids whose structure is based on DHT. The other enzyme, or type-2, 5-alpha reductase, predominates in the prostate gland, seminal vesicles (where sperm is produced and matures), epididymis, liver, and hair follicles. In the recent article, I pointed out that a simple way to deal with the increased production of DHT (4 to 8 percent of testosterone is converted via 5AR to DHT each day) is by using drugs designed to blunt the activity of 5AR. This results in a lowering of DHT, and a subsequent reduction or elimination of any side effects related to increased DHT production. This can include cardiovascular disease, prostate enlargement, acne, and erythrocytosis, or the excess production of red blood cells that can result from testosterone replacement therapy, particularly when injected forms are used.
Currently, two types of 5AR inhibiting drugs are approved for use. Both forms are used mainly to treat prostate enlargement, and they differ in their scope and activity. Dutasteride, sold under the trade name, Avodart, inhibits both forms of 5AR lowering the levels of circulating DHT by up to 97%. The other 5AR inhibitor, finasteride, comes in two potencies, 5 milligrams and 1 milligram. The 5-milligram dose, sold as Proscar, is used to treat prostate enlargement, while the 1-milligram dose, sold as Propecia, is used to treat male pattern baldness. Avodart works on both forms of the 5AR enzyme, while the activity of finasteride is limited to the type-2 form found in hair follicles. When exposed to DHT, men with the genes for male pattern baldness undergo miniaturization of the hair follicles, thus producing baldness, even though the hair follicles remain, but are miniaturized. Finasteride, by blocking DHT production, causes scalp levels of DHT to drop by an average of 60%, which effectively halts the balding process. In rare cases, lost hair is restored as the hair follicles return to their normal size. However, this effect usually happens only in men in whom the balding process has recently started. For those with long-term hair loss, blood vessels that feed the hair . . .