Post Cycle Therapy (PCT) is a process designed to recover natural hormone production after anabolic-androgenic steroid usage or other performance-enhancing drugs which suppress natural hormone production. PCT helps a user maintain muscle gains achieved during a cycle, and alleviate the side effects associated with a suppressed endocrine system. The way a PCT should be performed depends on; the length of cycle, the compound/esters used, individual response, and the dosages used. 

It’s important to understand the basics on how this suppression occurs in the first place, to help understand the methods of recovering your endocrine system that will be discussed later.

The HPTA (Hypothalamic Pituitary Testicular Axis) is a network of endocrine glands that control testosterone production in the body. The HPTA monitors and regulates how much testosterone is produced and circulating at any given time. Your genetic blueprint (DNA) largely determines your maximum testosterone levels, but factors like age, diet, body composition, lifestyle, and physical activity also play key roles in your overall production.

The HPTA operates on a negative feedback loop, which adjusts testosterone production based on the body’s needs:

High testosterone levels → Production slows or stops.

Low testosterone levels → Production increases.

This feedback system, controlled by the hypothalamus (the “master” gland), ensures hormonal balance, or homeostasis. All endocrine glands use similar feedback mechanisms, but during PCT, the focus is on the HPTA’s loop. The hypothalamus is responsible for detecting high levels of Testosterone and thus stopping its production, however it’s important to mention excess Estrogen and other hormones, like progestins and prolactin, can also interfere, but these are less commonly involved.

The specifics on Testosterone production:

• The hypothalamus detects the need for testosterone and releases GnRH.
• GnRH signals the pituitary gland to release LH and FSH.
• LH and FSH instruct the testes to produce and release testosterone. This is the final step of testosterone production in the HPTA.

This is important because the methods used in PCT manipulate these specific hormones in order to boost testicular function. 

Important considerations for how PCT will be structured; the length of cycle, the compound/ester used, and the dosages used.

1. The length of the cycle – The longer anabolic steroids are used, the more the Leydig cells in the testes remain inactive. Over time, this inactivity makes it harder for these cells to respond to LH and also FSH stimulation. Studies show that once testosterone administration stopped, LH levels returned to normal within three weeks, but testosterone production in most subjects took much longer to recover, suggesting the Leydig cells become desensitised to LH. 
2. The compound/ester used – After a compound is injected into your body there is a particular clearance time before it (and its metabolites) have been removed from your body. Some compounds and their metabolites take longer to be metabolised by the body, meaning you’ll have to wait longer before starting PCT as they will continue to exert HPTA suppression after the last injection. Some compounds like Anavar (and Halotestin even) are known to be the most mildly suppressive on your HPTA, whereas compounds like Nandrolone and Trenbolone are known to be very suppressive due progestogenic activity. Additionally, the ester attached will also determine how long the compound is present in your body (they control the rate of release into your bloodstream). 4 half-lives the amount of drug (6.25%) is considered to be negligible regarding its therapeutic effects. Below is a general idea on how long it will take for each ester to clear.
   1. Acetate 3-4 day
   2. Propionate 3-4 days
   3. Phenylpropionate 5-6 days
   4. Isocaproate 14-16 days
   5. Enanthate 14-18 days
   6. Cypionate 14-20 days
   7. Decanoate 26-30 days
   8. Undecylenate 52-56 days
   9. Undecanoate 80-84 days
   10. IMPORTANT NOTES This doesn’t consider metabolite clearance. The rate of clearance of metabolites is correlated to FSH and LH recovery too. Particularly 19-nortestosterone derivatives will continue to be suppressive beyond the ester terminal half life. Ideally you should stop AAS administration for as long as possible to allow the most time for drug clearance. Some suggest beginning PCT when you begin to notice symptoms of hypogonadism, however it is ultimately up to your discretion. ALSO, if you are using a compound with multiple esters, choose the ester that has the longest clearance time. 
3. Individual response – Everyone reacts differently to anabolic-androgenic steroids, and HPTA suppression severity is no exception. Some experience little suppression or recover quickly, and some experience heavy suppression and take a while to recover. It is important to get regular blood work done to determine your individual response, as judging by how you feel may not paint an accurate picture. This variability comes down to genetics and how each individual’s HPTA responds to maintain hormonal balance.

What kind of compounds are used for PCT?

• Primary
  • SERMs (Selective Estrogen Receptor Modulators)
• Secondary
  • hCG (Human Chorionic Gonadotropin)
  • Aromatase Inhibitors (AIs)

SERMs (Selective Estrogen Receptor Modulators)

The two SERMs most used are Nolvadex (Tamoxifen) and Clomid (Clomiphene), while Raloxifene and Torem (Toremifene Citrate) are newer SERMs. They block estrogen activity in some tissues while enhancing it in others. This can lead to both positive and negative effects.

In PCT, SERMs act as estrogen antagonists at the pituitary gland, prompting it to release LH and FSH. These hormones kick start natural testosterone production, which high estrogen levels can suppress through the HPTA’s negative feedback loop. 

Here are some different studies that show the different efficacies of SERMs.

A study titled ‘The effect of selective estrogen receptor modulator administration on the hypothalamic-pituitary-testicular axis in men with idiopathic oligozoospermia’ concluded that Nolvadex and Toremifene had superior antiestrogenic effects on the HPTA than Raloxifene.

SERM	FSH (mIU/mL)	LH (mIU/mL)	Testosterone (ng/dL)	Sperm concentration (x 106 / mL)	Normal sperm forms (%)
Nolvadex (Tamoxifen)	5.72 to 8.42 (+47%)	4.54 to 7.84 (+72%)	496.59 to 763.34 (+53%)	32.08 to 41.94 (+30%)	18.91 to 31.64 (+67%)
Torem (Toremifene)	5.64 to 9.53 (+69%)	4.05 to 6.54 (+61%)	498.96 to 743.92 (+49%)	25.84 to 37.82 (+46%)	23.09 to 31.73 (+37%)
Raloxifene	6.39 to 6.87 (+7%)	4.18 to 4.75 (+13%)	583.55 to 604.35 (+3%)	27.01 to 32.64 (+20%)	14.72 to 21.86 (+48%)

A study titled ‘HORMONAL EFFECTS OF AN ANTIESTROGEN, TAMOXIFEN, IN NORMAL

AND OLIGOSPERMIC MEN’ demonstrated that daily administration of 150mg of Clomid (Clomiphene Citrate) raised endogenous Testosterone levels by approximately 150%, whereas 20 mg of Nolvadex (Tamoxifen Citrate) daily raised endogenous Testosterone levels by the same amount. The sample size of this study was only 10. 

SERMs have concerning side effects associated with them. They increase the risk of Ocular damage, blood clots and deep vein thrombosis. However this is more associated with longer term usages and higher dosages than used in PCT. Regardless, SERMs usage should be intelligently planned, and used sparingly to avoid these serious effects.

It’s common for people to run both Nolvadex and Clomid. This is because the metabolites of Nolvadex have a slightly higher affinity for the Estrogen Receptor-Beta, whereas Clomid has a higher affinity for the Estrogen Receptor-Alpha. This ensures maximum efficacy in HPTA restoration.

hCG

Human Chorionic Gonadotropin (hCG) mimics LH, which mentioned before is a hormone that stimulates the testes to produce testosterone. Since hCG is a LH mimetic, it signals the Leydig cells in the testes to increase testosterone production. However hCG can increase estrogen production by stimulating aromatase activity in the testes. Additionally since hCG is a LH mimetic the testes may become equally as desensitised to it.

Aromatase Inhibitors (AIs)

Examples include Aromasin (Exemestane), Arimidex (Anastrozole), and Letrozole (Femara). Instead of blocking estrogen’s effects at specific receptors like SERMs, AIs reduce total estrogen levels by inhibiting the aromatase enzyme, which converts androgens into estrogen.

By lowering circulating estrogen, AIs can positively influence the negative feedback loop, encouraging the production of LH and FSH and boosting testosterone levels. The way this occurs is explained above. AIs are often used to control estrogen spikes caused by hCG. However some AIs interact poorly with Nolvadex. Arimidex and Letrozol have decreased serum concentrations when combined with Nolvadex, whereas Aromasin does not. 

PCT examples

PCT protocols drastically vary between different experts and coaches. You shouldnt blindly follow a PCT example as the best PCT will factor in a variety of circumstantial factors. These examples should just give an idea of how PCT are typically structured, and are not recommendations.

• Original Power PCT – By Michael Scally (former) M.D, and found in Anabolics 10th Edition by William Llewellyn.
  • hCG – 2500 IU EOD – first 16 days
  • Clomid – 100 mg ED – split the dose ½ in the AM, ½ in the PM for the first 30 days
  • Nolvadex – 10 mg ED – entire 45 days

• Researchers in a study titled ‘Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin’ treated a 17 year old steroid abuser, with 10 000 IU of HCG weekly for one, then 5000 IU weekly for one month, then 2500 IU for one month, after 15 months of fortnightly sustain 250mg injections. His serum Testosterone levels returned to normal over the 3 months of treatment, with improvements in condition seen within the first week

• Dave Palumbo’s PCT
  • 2000 IUs of (HCG) E3D (every 3rd day) for the first two weeks
  • For the next two weeks, 50mg of Chlomid ED and 10mg Nolvadex bidaily 

• Vigorous Steve – Taken from Youtube Video Titled ‘Post-Cycle Therapy (PCT) Done The Right Way, The HPTA Way!! #shorts’
  • Recommends tapering down to a genuine TRT dosage after a cycle to acclimate yourself to the desired level of endogenous testosterone after PCT – with this TRT dosage acting as a ‘bridge’
  • This will be done whilst other steroids are metabolising from your system
  • Then he recommends stopping the TRT dosage until your Testosterone levels hit close to 0 ng/dl (hit a low point) and then begin HCG unless you were running HCG during cycle which you should continue using
  • Then start SERMS which have dosages which taper down over 4-6 weeks

• A study titled ‘Anabolic steroid-induced hypogonadism: diagnosis and treatment’ recommends:
  • Block work prior
  • For weeks 1-4,  a tapered course of TRT, and administration of a SERM (such as clomiphene citrate, 25 mg every other day). For those with AAS-induced gynecomastia, 10–20 mg tamoxifen daily 
  • Check blood work after this point
  • If the person has a poor gonadotropin/testosterone response, for the next 4 weeks use 1000-3000 IU hCG 3 times per week, with the same dosage of a SERM used in weeks 1-4. If a person gets gynecomastia from hCG consider Tamoxifen or Arimidex
  • Check blood work again at this point

Blood work:

Blood work, blood work, blood work. The most important thing for AAS users is to get regular blood work. Before starting, regularly whilst on cycle, and regularly during PCT.

References:

 Tsourdi E, Kourtis A, Farmakiotis D, Katsikis I, Salmas M, Panidis D. The effect of selective estrogen receptor modulator administration on the hypothalamic-pituitary-testicular axis in men with idiopathic oligozoospermia. Fertil Steril. 2009 Apr;91(4 Suppl):1427-30. doi: 10.1016/j.fertnstert.2008.06.002. Epub 2008 Aug 9. PMID: 18692782.

 Vermeulen A, Comhaire F. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Fertil Steril. 1978 Mar;29(3):320-7. doi: 10.1016/s0015-0282(16)43160-2. PMID: 640052.

 Gill GV. Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin. Postgrad Med J. 1998 Jan;74(867):45-6. doi: 10.1136/pgmj.74.867.45. PMID: 9538490; PMCID: PMC2360778.

 Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014 May;101(5):1271-9. doi: 10.1016/j.fertnstert.2014.02.002. Epub 2014 Mar 14. PMID: 24636400.