After the end of an anabolic androgenic steroid (AAS) cycle, the steroid user should estimate the half life of the particular esters he used.
This will define the correct timing of drug clearance in the system.
Depending on the slow or fast esters, one or two weeks approximately are required in order to eliminate the substance from the body.
The idea of the gradual reduction of injectable testosterone does not provide any benefit to the hormonal system.
It only reinforces the belief, that the user is still on a cycle.
Either one reduces the dose gradually or abruptly-cold turkey, the Hypothalamic Pituitary Testicular Axis (HPTA) is shut off from day one (when testosterone is used).
The first phase of PCT involves the administration of the peptide of beta-human chorionic gonadotropin (beta-HCG), which ensures the stimulation of HPTA.
HCG is produced from the placenta after implantation, during the early stages of pregnancy.
Actually prediction test of pregnancy is checked out by serum, or urine levels of HCG.
It is a mimicker-analogue of luteinizing hormone (LHRH), which stimulates endogenous testosterone production in the Leydig cells of the testicles.
It is obvious that HCG, as a gonadotropin, will inhibit GnRH in the hypothalamus.
It helps during primary hypogonadism, where hypophysis is active (LH/FSH normal or high levels), while Total (TT) and Free Testosterone (FT) are low.
All AAS suppress the HPTA.
Therefore, the endogenous testosterone production is reduced significantly (homeostatic mechanism).
The use of HCG permits testicles and scrotum to keep their volume and triggers endogenous testosterone production.
The usual protocol provides the intramuscular-subcutaneous injections of 1500 IU every third day (72 hours) for two, or three weeks.
Usually the dosage of 5000 IU is used for cases of cryptorchidism in boys who have not yet entered puberty.
Initially all AAS users suffer from primary hypogonadism, which gradually turns into secondary (late onset).
Abuse of beta hCG (> 5000 IU) and its extensive use (over four weeks) will cause testicle whipping and saturation of LH receptors.
The resulting rise in natural testosterone will inhibit its own production on the hypothalamus and pituitary gland and eventually will have a negative impact.
The prolonged HCG abuse for over four weeks could lead to high levels of estradiol with peripheral edema, gynecomastia, and weight gain, mood swings with emotional instability and headaches due to increased intracranial pressure from water retention.
We should concern that a peptide from chemical point of view, does not aromatise.
However, as LH will increase endogenous testosterone production, this testosterone will eventually get aromatised.
The second phase of PCT involves clomiphene citrate, a medication belonging to the class of Selective Estrogen Receptors Modulators (SERMs).
This compound acts half estrogenic and the other half as anti-estrogenic.
It actually occupies the estrogenic receptor, so that the floating estrogens are not capable of getting attached to their receptor.
Clomiphene’s actual action is to trick hypothalamus, by giving the sensation of decreased estrogens.
The drop in estrogens would signal for GnRH release from hypothalamus, thus stimulating LH & FSH production from hypophysis.
Therefore, we realise that this mechanism is opposite than how beta-HCG works.
Along with clomiphene citrate, another SERM (tamoxifen citrate) can also be used simultaneously.
It lowers beta estradiol (E2) in the blood and this is a positive signal for GnRH and LH, FSH production.
SERMs are also used for two to three weeks long.
Tapering is the usual dosage (50mg=>25mg & 20mg=>10mg).
The fact that clomiphene acts estrogenically to other tissues (brain) explains the fact that the medication may cause dysthymia (moodiness).
In the liver, aromatisation by SERMs improves atheromatic profile and ratio of lipoproteins HDL/LDL.
Occasionally, after the discontinuation of SERMs, estrogens might rise.
Aromatase inhibitors (AIs) are a class of drugs used in breast cancer.
Inhibiting the action of the enzyme aromatase, which converts androgens into estrogens, AIs suppress estrogen production and are considered potent anti estrogens.
The two types of AIs include irreversible steroidal inhibitors, such as exemestane and non-steroidal inhibitors, such as anastrozole and letrozole.
In a study held by Greeks, 1mg/day of anastrozole or 2.5 mg/day of letrozole for 6 months could elevate LH and TT, through lower beta estradiol (E2).
Letrozole is even more potent than anastrozole, while exemestane is considered to be a suicidal AI.
However, AIs abuse will crush on E2, which will have reverse effects in libido.
A small amount of estrogens is required for proper sexual drive.
Besides, AIs abuse will have a negative impact on high-density lipoprotein (HDL) and bone mineral density (BMD).
Joints also tend to ache, due to less lubrication.
SERMs are better to be taken prior to bed time, since hormonal production takes place during night sleep.
After PCT is through, a period of OCT (off cycle therapy),could follow with a wide variety of different substances and antioxidant agents: (glutathione, NAC, ALA, milk thisle, beta carotene, ascorbate, tocopherol, selenium, Q10, lycopene, godji, Liv 52, acai, saw palmeto, omega 369, niacin, statins, phytosterols, garlic, ARA, beta alanine, DAA, ZMA, Vit D3 and creatine monohydrate).
Tocopherol (vitamin E) improves sperm quality by increasing the mobility of sperm cells, but not their absolute number.
Injectable cyanocobalamin (B12) along with folic acid and betaine will lower homocysteine, a substance linked to cardiovascular disease.
Furthermore, it will help to yield with the DNA synthesis and the enhancement of hematopoiesis (increase of Hgb, Htc).\
Cholesterol rich foods (as red meat and egg yolk) could contribute to a better hormonal profile, since steroid hormones production begins from the steroid molecule of cholesterol.
Regarding spermatogenesis and seminal fluid production, it’s a process hindered while on steroid cycles.
After all, AAS lead to permanent infertility.
Oligospermia is defined as the small amount of sperm (<20million spermatozoa/ml).
Azoospermia is a clinical condition which is equivalent to sterility, as there is a complete lack of spermatozoa.
The clinical diagnosis comes after two continued seminal fluid measurements, with a three month difference between them.
There is a strong suppression of the follicle stimulating hormone (FSH).
All of AAS users, who wish to follow a competitive career, should undergo hormone tests and a semen analysis.