Laws and Penalties: Concerns over growing illegal AAS abuse by teenagers, and many of the just discussed long-term effects, led Congress in 1991 to place the whole AAS class of drugs into Schedule III of the Controlled Substances Act (CSA). Under this legislation, AAS are defined as any drug or hormonal substance, chemically and pharmacologically related to T (other than estrogens, progestins, and corticosteroids) that promotes muscle growth. The possession or sale of AAS without a valid prescription is illegal. Since 1991, simple possession of illegally obtained AAS carry a maximum penalty of one year in prison and a minimum $1,000 fine if this is an individual’s first drug offense. The maximum penalty for trafficking (selling or possessing enough to be suspected of selling) is five years in prison and a fine of $250,000 if this is the individual’s first felony drug offense. If this is the second felony drug offense, the maximum period of imprisonment and the maximum fine both double. While the above listed penalties are for federal offenses, individual states have also implemented fines and penalties for illegal use of AAS. State executive offices have also recognized the seriousness of AAS abuse and other drugs of abuse in schools. For example, the State of Virginia enacted a law that will allow student drug testing as a legitimate school drug prevention program (48, 49).
A 31-year-old man presenting with an 18-month history of sexual dysfunction resulting from severe adult-onset IHH (LH U/L, FSH U/L, T nmol/L). Initial therapy with 50 mg of clomiphene citrate (CC) three times a day for 7 days, with overnight LH pulse profiling and 9 am T levels evaluated at baseline and on completion. A 2-month washout period, followed by low-dose maintenance therapy (25-50 mg/d) for 4 months.
MAIN OUTCOME MEASURE(S):Baseline and stimulated T levels and LH pulsatility; effect on sexual function.
RESULT(S):Clomiphene therapy resulted in complete normalization of pulsatile gonadotropin secretion, serum T level, and sexual function. CONCLUSION(S):Isolated hypogonadotropic hypogonadism may result from an acquired defect of enhanced hypothalamic sensitivity to E-mediated negative feedback. Whereas direct T replacement therapy can further suppress endogenous gonadotropin secretion, treating IHH men with gonadotropins can stimulate endogenous T secretion and enhance fertility potential. On theoretical grounds, reversal of gonadotropin deficiency with CC might be expected to have a similar biological effect.