T Nation

The Final Word on PCT?



pretty interesting although obviously as stated in the article there is no way any bodybuilder was really taking those paltry doses to begin with....regardless very good info


Never heard of triptorelin


Read that the other day, definitely a point of interest to our community.


Saw this the other day. I'd be interested to know if anyone has any ideas about how this works. From the limited amount I've read, the effect of a GnRH agonist is to cause a sudden increase in FSH and LH secretion followed by receptor downregulation (and a decrease in LH and FSH) about 10 days later. Presumably it is that "flare effect" which works for our purposes?


To add to the discussion, I found this in one of my files. It was in an article called "Initial hormone therapy for metastatic prostate cancer"


Mechanism of action â?? Medical castration using a gonadotropin releasing hormone (GnRH) agonist was first reported in 1982 [17] . Synthetic GnRH analogs have greater receptor affinity and reduced susceptibility to enzymatic degradation compared to the natural GnRH molecule, and are approximately 100-fold more potent [18] . GnRH (also termed luteinizing hormone releasing hormone [LHRH]) agonists bind to the GnRH receptors on pituitary gonadotropin-producing cells, causing an initial release of both luteinizing hormone (LH) and follicle stimulating hormone (FSH), which causes a subsequent increase in testosterone production from testicular Leydig cells (show figure 1).

After about one week of therapy, GnRH receptors are down-regulated on the gonadotropin-producing cells, with a decline in the pituitary production of LH and FSH [19] . The fall in serum LH leads to a decrease in serum testosterone to castrate levels within three to four weeks after the start of treatment [20] . Continued treatment maintains serum testosterone at castrate levels.

The decrease in testosterone production is generally reversible upon cessation of GnRH agonist therapy. However, testosterone production does not always return to baseline levels and may be related to the duration of GnRH agonist therapy, patient age, and other factors [21,22] .

The transient rise in LH when GnRH therapy is initiated can cause a surge in serum testosterone, which may stimulate prostate cancer growth. This "flare" may cause an increase in bone pain, bladder obstruction, or other symptoms due to prostate cancer [23] . Thus, initial treatment with GnRH alone is contraindicated in men with severe urinary tract obstruction or painful bone metastases.

The flare phenomenon can be effectively prevented with antiandrogen therapy, which blocks the effect of the increased serum testosterone [12] . A placebo-controlled trial demonstrated that antiandrogens decrease bone pain at the initiation of GnRH agonists for patients with metastatic prostate cancer [24] . In practice, antiandrogen therapy is often started seven days prior to GnRH agonist initiation for men at high risk of flare symptoms, or concurrently for asymptomatic patients. Antiandrogen therapy is then continued for two to four weeks.


And about Triptoelin itself:

Triptorelin: Drug information

U.S. BRAND NAMES â?? Trelstar® Depot; Trelstar® LA

Gonadotropin Releasing Hormone Agonist

DOSING: ADULTS â?? Advanced prostate carcinoma:

Trelstar® Depot: 3.75 mg once every 28 days

Trelstar® LA: 11.25 mg once every 84 days

DOSING: ELDERLY â?? Refer to adult dosing.

DOSING: RENAL IMPAIRMENT â?? Specific guidelines are not available.

DOSING: HEPATIC IMPAIRMENT â?? Specific guidelines are not available.

DOSAGE FORMS â?? Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Injection, powder for reconstitution:
  Trelstar® Depot: 3.75 mg [contains polylactide-co-glycolide; polysorbate 80]
  Trelstar® LA: 11.25 mg [contains polylactide-co-glycolide; polysorbate 80]

Injection, powder for reconstitution:
  Trelstar® Depot: 3.75 mg
  Trelstar® LA: 11.25 mg


ADMINISTRATION â??  Administer by I.M. injection into the buttock; alternate injection sites.

USE â?? Palliative treatment of advanced prostate cancer as an alternative to orchiectomy or estrogen administration

USE - UNLABELED / INVESTIGATIONAL â?? Treatment of endometriosis, growth hormone deficiency, hyperandrogenism, in vitro fertilization, ovarian carcinoma, pancreatic carcinoma, precocious puberty, uterine leiomyomata

ADVERSE REACTIONS SIGNIFICANT â?? As reported with Trelstar® Depot and Trelstar® LA; frequency of effect may vary by product:

  Central nervous system: Headache (30% to 50%)
  Endocrine & metabolic: Hot flashes (95% to 100%), glucose increased
  Hematologic: Hemoglobin decreased, RBC count decreased
  Hepatic: Alkaline phosphatase increased, ALT increased, AST increased
  Neuromuscular & skeletal: Skeletal pain (12% to 13%)
  Renal: BUN increased

1% to 10%:
  Cardiovascular: Leg edema (6%), hypertension (4%), chest pain (2%), peripheral edema (1%)
  Central nervous system: Dizziness (1% to 3%), pain (2% to 3%), fatigue (2%), insomnia (2%), emotional lability (1%)
  Dermatologic: Rash (2%), pruritus (1%)
  Endocrine & metabolic: Tumor flare (8%), alkaline phosphatase increased (2%), breast pain (2%), gynecomastia (2%), libido decreased (2%)
  Gastrointestinal: Nausea (3%), anorexia (2%), constipation (2%), dyspepsia (2%), vomiting (2%), abdominal pain (1%), diarrhea (1%)
  Genitourinary: Impotence (2% to 7%), dysuria (5%), urinary retention (1%), urinary tract infection (1%)
  Hematologic: Anemia (1%)
  Local: Injection site pain (4%)
  Neuromuscular & skeletal: Leg pain (2% to 5%), back pain (3%), arthralgia (2%), leg cramps (2%), myalgia (1%), weakness (1%)
  Ocular: Conjunctivitis (1%), eye pain (1%)
  Respiratory: Cough (2%), dyspnea (1%), pharyngitis (1%)

Postmarketing and/or case reports (limited to important or life-threatening): Anaphylaxis, angioedema, hypersensitivity reactions, pituitary apoplexy, renal dysfunction, spinal cord compression

CONTRAINDICATIONS â?? Hypersensitivity to triptorelin or any component of the formulation, other LHRH agonists or LHRH; pregnancy

Special handling: Hazardous agent: Use appropriate precautions for handling and disposal.

Concerns related to adverse effects: Hypersensitivity reactions: Angioedema and anaphylaxis have rarely occurred. Pituitary apoplexy: Rare cases of pituitary apoplexy (frequently secondary to pituitary adenoma) have been observed with leuprolide administration (onset from 1 hour to usually <2 weeks); may present as sudden headache, vomiting, visual or mental status changes, and infrequently cardiovascular collapse; immediate medical attention required. Spinal cord compression: Cases of spinal cord compression have been reported with LHRH agonists; observe patients with metastatic vertebral lesions closely. Tumor flare: Transient increases in testosterone can lead to worsening symptoms (bone pain, hematuria, bladder outlet obstruction) of prostate cancer during the first few weeks of therapy.

Disease-related concerns: Urinary tract obstruction: Observe patients with urinary tract obstruction closely.

Special populations: Pediatrics: Safety and efficacy have not been established in children.

Antidiabetic Agents: Luteinizing Hormone-Releasing Hormone Analogs may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy

PREGNANCY RISK FACTOR â?? X (show table)

PREGNANCY IMPLICATIONS â?? Contraindicated in women who are or may become pregnant.

LACTATION â?? Excretion in breast milk unknown/contraindicated

MONITORING PARAMETERS â?? Serum testosterone levels, prostate-specific antigen

CANADIAN BRAND NAMES â?? Trelstar®; Trelstar® Depot; Trelstar® LA

INTERNATIONAL BRAND NAMES â?? Arvekap (GR); Decapeptyl (AE, AR, BE, BG, BH, CL, CN, CO, Cy, CZ, DE, EC, EG, ES, FR, GB, HK, HN, HR, HU, IE, IL, IQ, IR, IT, JO, KW, LB, LU, LY, MY, NL, OM, PE, PL, PT, PY, QA, SA, SY, UY, VE, YE); Decapeptyl CR (AE, BH, Cy, EG, IL, IQ, IR, JO, KP, KW, LB, LY, MY, OM, PH, QA, SA, SY, TH, TW, YE); Decapeptyl Depot (AT, CZ, DE, DK, EE, FI, KP, MY, SE); Decapeptyl LP (FR); Decapeptyl Retard (CH); Decapeptyl SR (PK); Diphereline (PL); Diphereline PR (HK, TW); Diphereline S.R. (PL); Gonapeptyl (FR, GB, IE); Gonapeptyl Depot (BR); Neo Decapeptyl (BR); Pamorelin (NO)

MECHANISM OF ACTION â?? Causes suppression of ovarian and testicular steroidogenesis due to decreased levels of LH and FSH with subsequent decrease in testosterone (male) and estrogen (female) levels. After chronic and continuous administration, usually 2-4 weeks after initiation, a sustained decrease in LH and FSH secretion occurs.

Absorption: Oral: Not active

Distribution: Vd: 30-33 L

Protein binding: None

Metabolism: Unknown; unlikely to involve CYP; no known metabolites

Half-life elimination: 2.8 +/- 1.2 hours
  Moderate-to-severe renal impairment: 6.5-7.7 hours
  Hepatic impairment: 7.6 hours

Time to peak: 1-3 hours

Excretion: Urine (42% as intact peptide); hepatic

PATIENT INFORMATION â?? Use as directed. Do not miss monthly appointment for injection. You may experience disease flare (increased bone pain), blood in urine, and urinary retention during early treatment (usually resolves within 1 week). Hot flashes are common; you may feel flushed and hot (wearing layers of clothes or summer clothes and cool environment may help). If it becomes annoying and bothersome, let prescriber know. Report irregular or rapid heartbeat, unresolved nausea or vomiting, numbness of extremities, breast swelling or pain, difficulty breathing, or infection at injection sites.


I read gnrh agonists are used in the treatment of acromegaly also because they cause downregulation, as mentioned. Maybe if the drug is used like hcg, not constantly to avoid downregulation, it would be helpful.


oh my fucking god, to think i'll never have to sufffer the emotional roller-coaster of SERMS and the concomitant acne flare up which encrusts my face in volcanic puss.... gasp

licence to thrill


Has anyone managed to read the article listed in full? I have only come across an abstract or the option to pay $30 for a pdf of it. The only articles I have found using triptorelin are in treatment of prostate or ovarian cancer.

As Rational mentioned, the flare is the part which seems to have an appeal to the forum. However, as downregulation is obviously an issue, how would the dosing go? I see from the original article that it seems a one type shot kickstarted the system. Do you think that estrogen control during the kickstart would still be an issue? In other words, would you need to still need to take Nolva or something as per normal.

I guess I am seeing this as a possible way to smooth out PCT rather than replace it. Of course, I am just thinking out loud without having read the actual study. It does seem to be quite interesting on the face of it.


If you want to use an untested chemical for PCT, I'd suggest fulvestrant. It's a SERM like nolvadex, but it's a once a month injection. It not only blocks estrogen receptors, like nolvadex, but also downregulates estrogen receptors, so you're less likely to get gyno. It's also is the only full estrogen antagonist. SERMs all have mixed agonist/antagonist (estrogen/antiestrogen) effects. The dose is also naturally tapered, like enanthate estered drugs.

Right now the only was to get fulvestrant is from a pharmacy. It costs like $1000 for one injection. Chemically, it doesn't look much different than nolvadex or clomid. I bet it'd be much easier to produce than peptide drugs. The only reason why it costs $1000 is because of the patent hasn't run out yet, and there isn't enough demand in the market for underground labs to produce it.



The down regulation occurs because of the overstimulation of receptors - the dose used in prostrate cancer is around 100 x that used in the study. The smaller dose utilised by the Drs in the study is enough to excite receptors and get them working but not enough to continually overstimulate for an extended period and down regulate


It occurred to me that this might have an application to TRT as well. I wonder how it would affect someone whose system is running at less than peak capacity. In other words, would someone with low test see any kind of recovery of normal levels?

On the face of it, it seems logical. The bodybuilder in the study wasn't going through PCT or a temporary downregulation, he was damaged. His system just wasn't working. Yet, apparently, the shot got him up and running again. While his actions may have put him in the same place as the folks on the T Replacement forum find themselves, would they not see a benefit from something like this?


Thanks, that makes a lot of sense. I wonder whether this kind of protocol would work well with a test taper...


I can access the full text version. Don't really want to repost the whole thing even tho it is a very short article. The discussion relates more to how easy it is to purchase AAS and the state of his hormone levels aswell as a brief history of PED's.

"Our patient showed no spermatogenesis dysfunction, even though he had used anabolic steroids for over a decade. This could be explained by his periodic self-administered treatment with clomiphene citrate and human chorionic gonadotropin between the cycles of steroids. Clomiphene is a selective estrogen receptor modulator that blocks the feedback inhibition of estradiol at the level of the hypothalamus, thus increasing pituitary release of both LH and follicle-stimulating hormone (5) and (21). In addition, clomiphene decreases the conversion of androgen substrate to estrogen by aromatase inhibition (22). It is this ability to block estrogen that leads to its postcycle use by bodybuilders to reduce the development of gynecomastia after self-administration of androgen drugs. Clomiphene is extensively used in the induction of ovulation (23), but it has also been used to reverse hypogonadotropic hypogonadism in many conditions like falciform anemia, uremia, and alcohol abuse, and it stimulates gonadotropin secretion in patients with sulpiride-induced hyperprolactinemia and gonadotropin suppression 24 J.T.T. Bjork, R.R. Varma and H.I. Borkowf, Clomiphene citrate therapy in a patient with Laennec's cirrhosis, Gastroenterology 72 (1977), pp. 1308â??1311. View Record in Scopus | Cited By in Scopus (2)(24)."

"The cycles of pituitary stimuli with clomiphene and human chorionic gonadotropin could also explain why our patient did not exhibit the hypothalamic-pituitary dysfunction that had been clinically evident previously."

PIROLA, I.; C. CAPPELLI; A. DELBARBA; T. SCALVINI; B. AGOSTI; D. ASSANELLI; A. BONETTI and M. CASTELLANO. Anabolic steroids purchased on the Internet as a cause of prolonged hypogonadotropic hypogonadism. Fertility and Sterility, In Press, Corrected Proof.


Absolutely correct. : )