HPGA Normalization Protocol After Androgen Treatment
N Vergel, AL Hodge, MC Scally
Program for Wellness Restoration, PoWeR
Objective Results Discussion
To develop an approach to cycle androgens that would result in significant changes in body composition and accelerate the normalization of the hypothalamic pituitary gonadal axis (HPGA) after cessation of androgens.
Methods
An uncontrolled study of 19 HIV-negative eugonadal men, ages 23 – 57 years, administered testosterone cypionate and nandrolone decanoate for 12 weeks, and then were treated simultaneously with a combined regimen of human chorionic gonadotropin (hCG) (2500 IU/QODx16d), clomiphene citrate (50 mg PO BID x 30d) and tamoxifen (20 mg PO QD x 45d), to restore the HPGA.
Results
Mean FFM by DEXA increased from 64.1 to 69.8 kg (p<.001); percent body fat decreased from 23.6 to 20.9 (p<.01); strength increased significantly from 357.4 lb to 406.4 lb (p=.02). No significant changes in serum chemistries and liver function tests were found. HDL-C decreased from a mean value of 44.3 to 38.0 (p=.02). Mean values for luteinizing hormone (LH) and total testosterone (T) were 4.5 and 460, respectively prior to androgen treatment. At the conclusion of the 12-week treatment with androgens the mean LH <0.7 (p<.001) and total testosterone was 1568 (p<.001). The mean values after treatment with the combined regimen were LH=6.2 and testosterone=458.
Discussion
The use of androgens has been reported to improve lean body mass, strength, sexual function, and mood accompanied by side effects caused by continuous uninterrupted use of these compounds (polycythemia, testicular atrophy, hypertension, liver dysfunction [oral androgens] and alopecia.) Androgen-induced HPGA suppression causes a severe hypogonadal state in most patients that often require an extensive period of considerable duration for normalization. This prevents most if not all individuals from cycling off these medications due to the adverse impact of this state on their previously gained LBM and quality of life. The protocol of hCG-clomiphene-tamoxifen was successful in restoring the HPGA within 45 days after androgen cessation. Further controlled studies are needed to determine if these results can be duplicated in HIV positive subjects.
PRACTICAL APPLICATION
The esters used in the abstract were cypionate and deconate however the administration of the PCT medications were started the day after aas cessation. Essentially the aas esters were still active when PCT began. The first 16 days a large amount of HCG was used in order to increase the mass of the testes so that they could sustain output of testosterone sooner. The HCG was stopped about the time the esters cleared so that estrogenic activity from the HCG would be reduced. During those first 16 days 2 different SERM’s were also employed (Clomid and Nolvadex) This protocol is contrary to what is typically recommended in many forums but regardless the protocol was effective in all 19 men. This is a 100% success rate! After the HCG was discontinued both SERM’s were continued. The following is the exact protocol in laymen’s terms.
Day 1-16 : 2500iu HCG every other day.
Day 1-30 : Nolva 20mg/day; Clomid 100mg/day (50mg was taken twice per day)
Day 31-45 : Nolva 20mg/day
I now strongly believe that an AI should be used as long as there is an aromatizing compound being administered. In this case Testosterone and HCG aromatize therefore using an AI until these meds clear is now what I am recommending. There is some evidence that adding Nolva to an AI does not increase the effectiveness of estro control therefore Nolva has no real advantage alongside an AI unless one is experiencing gyno. Additionally Nolva has been shown to reduce IGF-1 and GH levels. This is not a big deal on cycle as testosterone increases IGF-1 in a dose dependant relationship. However off cycle this is a problem. PCT is a fragile time and lower IGF-1 and GH levels is not desireable as I am sure you can appreciate. The last few days I have been relooking at AI's to find one that is specific to men that can be used on cycle and during PCT. It is my conclusion that Aromasin is the obvious choice.
Aromasin (Exemestane) is a Type-I aromatase inhibitor, or suicidal aromatase inhibitor. It’s called this because it lowers estrogen production in the body by attaching to the aromatase enzyme, and permanently deactivating it. (1)
Personally, I find this to be a very interesting mechanism of action when compared to type-II aromatase inhibitors, which bind competitively to the aromatase enzyme, and eventually unbind, rendering it active again. In the case of Aromasin, this doesn’t happen, and once it does its job on the enzyme, those particular enzymes will no longer function.
Because the enzyme is permanently deactivated there is no estrogen rebound with Aromasin. Estrogen rebound at this critical time during PCT is undesirable so using Arimidex would be inferior. Therefore I believe Aromasin is the AI of choice during PCT.
Reference:
1. A predictive model for exemestane pharmacokinetics/pharmacodynamics incorporating the effect of food and formulation.Br J Clin Pharmacol. 2005 Mar;59(3):355-64.
The following is a study done in men with Aromasin that shows significant effect on estrogen and testosterone; Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14–26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P 0.002); 50 mg, 32% (P 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 ± 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.
Jokes aside wish you all the best in achieving sobriety. You will feel amazing at first but the feeling fades quick. So one day at a time and use training for those hard days. GL and stay strong mentally brother 
