This is cut&pasted from a post by Dr. Albers:
For my thesis I referenced an abstract of restoration of the HPG axis induces by AAS abuse by Scally and Street. Keep in mind that an abstract is not peer reviewed, it was just presented on the ACSM congress 2000. On the other hand Chris Street seems to be quite a reliable source for me.
Abstract 798 MSSE Suppl 2000
Pharmaceutical intervention of anabolic steroid induced hypogonadism our success at restoration of the hpg axis
Scally C, Street C
High-dose anabolic-androgenic steroid (AAS) administration results in hypogonadotropic hypogonadism (HH). Physical manifestations can include one or more of the following: depression, decreased sexual desire, impotence, feelings of apathy, testicular atrophy, and loss of muscle mass and strength. Due to feedback inhibition, laboratory values drop well below established physiologic norms: leutinizing hormone (LH) > 3.6 IU/L, follicle stimulating hormone (FSH) > 2.25 IU/L, and testosterone y 300 ng/dL. A search of the literature reveals an absence of studies dealing specifically with AAS-induced HH, and restoration of normal endocrine function.
We report on two interesting cases of AAS using bodybuilders who were brought out of the hypogonadal state. Blood samples were taken in the morning for both subjects and analysed using chemiluminescence (Quest diagnostics, Irving, TX). Post therapy samples were taken 15 days after the last HCG injection.
Case I: 60 206 lbs., 33 years old Caucasian male with a 10+ year history of steroid-administration for bodybuilding and Powerlifting. By his own admission he was a heavy user, taking from 500 mg/week to 2+ grams/week. Pre-treatment values: LH>1.0 IU/L, T 191 ng/dL. One course of therapy (32 days) was given: 2,500 IU of HCG every 4 days (8 injections total), 50 mg clomifen bid and 10 mg tamoxifen qd. Despite massive drug use patient was an exceptionally good responder. Post-treatment values: LH 5.2 IU/L, T 1072 ng/dL.
Case 2: 510 184 lbs, 36 years old Caucasian male with a 2 year history of continuous nandrolone use (200-400 mg/week). Pre treatment values: LH >1.0 IU/L, T 45 ng/dL. Treatment I (32 days): 2,500 IU HCG every 4 days (8 total), clomifen 50 mg bid, arimidex 1 mg qd. Post values: LH > 1.0 IU/L, T 38 ng/dL. Treatment 2 (60 days): 5,000 IU HCG every 4 days (4 inj. total), followed by 2,500 IU HCG every 4 d (4 inj. total), clomifen (50 mg bid) and tamoxifen (10 mg qd). Post-values: LH > 1.4 IU/L, T 63 ng/dL. Treatment 3 (32 days): 5,000 IU HCG qod (6 inj. total) followed by 2,500 IU HCG qod (6 inj. total) given simultaneously with menotropins 150 IU qod (6 inj. total), clomifen (50 mg bid) and tamoxifen (10 mg bid). Post-values: LH 9.8 IU/L, T 507 ng/dL.
Restoration of the HPG axis, even in severe cases of hypogonadism, is possible with combined therapies and careful monitoring of the patient. With continued popularity of these drugs, long-term androgen deficiency is a health concern for former AAS users. Further research is needed in this area.
For my thesis I referenced an abstract of restoration of the HPG axis induces by AAS abuse by Scally and Street. Keep in mind that an abstract is not peer reviewed, it was just presented on the ACSM congress 2000. On the other hand Chris Street seems to be quite a reliable source for me.
Abstract 798 MSSE Suppl 2000
Pharmaceutical intervention of anabolic steroid induced hypogonadism our success at restoration of the hpg axis
Scally C, Street C
High-dose anabolic-androgenic steroid (AAS) administration results in hypogonadotropic hypogonadism (HH). Physical manifestations can include one or more of the following: depression, decreased sexual desire, impotence, feelings of apathy, testicular atrophy, and loss of muscle mass and strength. Due to feedback inhibition, laboratory values drop well below established physiologic norms: leutinizing hormone (LH) > 3.6 IU/L, follicle stimulating hormone (FSH) > 2.25 IU/L, and testosterone y 300 ng/dL. A search of the literature reveals an absence of studies dealing specifically with AAS-induced HH, and restoration of normal endocrine function.
We report on two interesting cases of AAS using bodybuilders who were brought out of the hypogonadal state. Blood samples were taken in the morning for both subjects and analysed using chemiluminescence (Quest diagnostics, Irving, TX). Post therapy samples were taken 15 days after the last HCG injection.
Case I: 60 206 lbs., 33 years old Caucasian male with a 10+ year history of steroid-administration for bodybuilding and Powerlifting. By his own admission he was a heavy user, taking from 500 mg/week to 2+ grams/week. Pre-treatment values: LH>1.0 IU/L, T 191 ng/dL. One course of therapy (32 days) was given: 2,500 IU of HCG every 4 days (8 injections total), 50 mg clomifen bid and 10 mg tamoxifen qd. Despite massive drug use patient was an exceptionally good responder. Post-treatment values: LH 5.2 IU/L, T 1072 ng/dL.
Case 2: 510 184 lbs, 36 years old Caucasian male with a 2 year history of continuous nandrolone use (200-400 mg/week). Pre treatment values: LH >1.0 IU/L, T 45 ng/dL. Treatment I (32 days): 2,500 IU HCG every 4 days (8 total), clomifen 50 mg bid, arimidex 1 mg qd. Post values: LH > 1.0 IU/L, T 38 ng/dL. Treatment 2 (60 days): 5,000 IU HCG every 4 days (4 inj. total), followed by 2,500 IU HCG every 4 d (4 inj. total), clomifen (50 mg bid) and tamoxifen (10 mg qd). Post-values: LH > 1.4 IU/L, T 63 ng/dL. Treatment 3 (32 days): 5,000 IU HCG qod (6 inj. total) followed by 2,500 IU HCG qod (6 inj. total) given simultaneously with menotropins 150 IU qod (6 inj. total), clomifen (50 mg bid) and tamoxifen (10 mg bid). Post-values: LH 9.8 IU/L, T 507 ng/dL.
Restoration of the HPG axis, even in severe cases of hypogonadism, is possible with combined therapies and careful monitoring of the patient. With continued popularity of these drugs, long-term androgen deficiency is a health concern for former AAS users. Further research is needed in this area.
