Below is a read/study conducted by Dr Michael Scally. Some may contest that it's out dated info, I'll disagree with that notion!The famous PoWeR PCT Program by Dr. Michael Scally
There's a NEW'er version available, I'll post that soon enough.
After this study, I will also include a Protocol/advice on PCT by Dr Swale.
The PoWer PCT study ABSTRACT: AEGIS Security & Investigations - Los Angeles Private Investigator
A more detailed ABSTRACT in PDF: http://www.medibolics.com/ScallyVergelAstractHPGA.pdf
(HYPOTHALAMIC PITUITARY GONADAL AXIS NORMALIZATION PROTOCOL AFTER ANDROGEN TREATMENT)
The PoWeR PCT Program
The PCT program outlined below represents what I consider to be an ideal and effective post-cycle program. It was developed by the doctors at the Program for Wellness Restoration (PoWeR), who have a formidable history helping patients recover normal hormonal functioning following steroid therapy. One of the key doctors on this program, Dr. Michael Scally, claims to have successfully treated more than 100 cases of hypogonadism/hypogonadotrophic hypogonadism, and is very well known in the field of androgen replacement therapy. PoWeR published this program as part of a recent clinical study, which involved 19 healthy male subjects who were taking supraphysiological (highly suppressive) doses of testosterone cypionate and nandrolone decanoate for 12 weeks. Their HPGA Normalization Protocol focuses on the combined use of HCG, Nolvadex' and Clomid, and is perhaps the only clinically documented post-cycle therapy program to be found in the medical literature (it is amazing how little attention has been paid to hormone normalization in clinical medicine). The most notable variation from a classic PCT stack, such that I have( been a longtime supporter of, is the combined use of two anti-estrogens. In this case I cannot say that there is disadvantage to such use; perhaps it is indeed the better option.
Examining the program closely, we note that the teste are hit hard with HCG at the onset of therapy. Its intake however, is limited to only 16 days. The doctor, undoubtedly recognize that when HCG is taken for too long or at too high a dosage, it can desensitize the LH receptor. This would only further exacerbate the post cycle problem, not help it. Anti-estrogens are used during and after HCG, with a dosage of 10 mg of Nolvadex and 100 mg of Clomid per day rounding out this compliment of drugs. Clomid is used for a shorter period of time than Nolvadex, likely because of the desensitizing effect it too' can have (on the pituitary gland) with continued use. Among other things, these two anti-estrogens will continue to foster LH release as testosterone levels start to go back up, as well as combat any potential estrogenic side effects that may be caused by HCG's up-regulation and testicular aromatase activity. Although in the first couple of weeks the anti-estrogens probably do very Iittlle as they should be much more helpful towards the middle and end of the program. During this clinical investigation: normal hormonal function was restored in all subjects,I within 45 days of drug cessation. This is a definite success far more favorable than the protracted recovery window noted in studies without post-cycle therapy, such as the 250 mg/week testosterone enanthate investigation, highlighted in Figure I. For me, I believe such a detailed recovery program should follow any serious steroid cycle It is the best way to maintain your gains at their maximun and that is, after all, what we are after.
According to Dr. Michael Scally, the protocol described in Llewelly?s book has been updated. ? But it has changed minimally, he said. ? Now I extend the hCG duration by using 2,000 IU, now 10 shots total. The tamoxifen is 20 MG PO BID.
About Dr. Michael Scally
Dr. Scally?s education includes a double degree major in Chemistry (1975) and Life Sciences (1975) from the Massachusetts Institute of Technology (M.I.T.) Cambridge, MA. Following, from 1975-1980, in the M.I.T. Division of Brain Sciences & Neuroendocrinology Dr. Scally researched and published investigations on neurotransmitter relationships.1 Dr. Scally's research included involvement and participation in the earliest studies detailing the role of tryptophan, serotonin, and depression. During this time, he entered the prestigious Health Sciences & Technology Program, a collaboration of M.I.T. and Harvard Medical School. In June 1980, Dr. Scally was awarded by Harvard Medical School a Doctorate of Medicine, M.D. Continuing his education, Dr. Scally trained at Parkland Memorial Hospital, Southwestern Medical School. Scally completed the first year of postgraduate medical residency in general surgery followed by postgraduate medical residency in anesthesiology.
Consultations. Contact Dr. Scally at email@example.com or firstname.lastname@example.org. Dr. Scally has personally cared for thousands of individuals using AAS, particularly for anabolic steroid-induced hypogonadism. DONATIONS ARE NEEDED AND APPRECIATED AT WWW.ASIH.NET.
Buy his book: http://www.amazon.com/Anabolic-Stero...6978014&sr=8-3
About William Llewellyn
William Llewellyn is a world-renowned foremost authority on anabolic substances and its effects on muscular performance. An accomplished research scientist, author, publisher, inventor, columnist, and company CEO in the field of sports nutrition and anabolic substances, Llewellyn has been featured in ESPN Magazine, Washington Post, Fox News Channel, ESPN Television, NPR News, ESPN Radio and other national and regional TV / Radio news programs.
In addition to writing the Anabolics books, Llewellyn also publishes Body of Science Magazine, a quarterly publication dedicated to the "understanding of sports enhancement." He writes a monthly column for Muscular Development, and has written numerous articles for other bodybuilding publications including Ironman Magazine, Exercise for Men Only, and Natural Muscle.
During his fifteen years of anabolic research, Llewellyn has made several important scientific discoveries. His latest discovery of arachidonic acid has been patented for its anabolic properties and its "use as a method of increasing skeletal muscle mass."
Buy his book: http://www.amazon.com/William-Llewel...t_at_ep_dpi_10
PoWeR : Program for Wellness Restoration website - http://www.powerusa.org
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.
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.
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.
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.
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.
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.