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Terapija poslije ciklusa - PCT

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Pedja Petrovic:

--- Quote ---conservative therapy (i.e. nothing
--- End quote ---

 ;) ;) ;) ;)
ooo yeahhhhhh
and its working  ;) ;) ;)

sele137:
PCT and HPTA Normalization   
by Michael C. Scally, M.D.

Q: I just recently finished a 7 day treatment of Clomid at 100 mg a day. prescribed by my endocrinologist. What is the best case scenario of this protocol?

Can you tell me more about Clomid and how it works?

If the Clomid did raise my testosterone levels, then what is the doctor going to do next? I assume if it didn't raise my levels then he is going to put me on testosterone replacement therapy (TRT).


A: Clomiphene is classified as a selective-estrogen receptor-modulator (SERM).

Tamoxifen is classified as an estrogen receptor blocker.

Arimidex, Aromasin, Femara are aromatiziation enzyme inhibitors.

Clomiphene is classified as a selective-estrogen receptor-modulator (SERM) due to its ability to compete with estradiol for estrogen receptors at the level of the hypothalamus. Clomiphene blocks the normal negative feedback of circulating estradiol on the hypothalamus, preventing estrogen from lowering the output of gonadotropin releasing hormone (GnRH). During clomiphene therapy, the frequency and amplitude of GnRH pulses increase and stimulate the pituitary gland to release more FSH and LH.

In turn, FSH and LH stimulate the testicles to produce more testosterone. LH and FSH then apparently stimulate the testicles to produce testosterone and sperm. Sperm volume and density are increased; however, clomiphene may not increase sperm maturation or motility. Testosterone is converted to estradiol as well as dihydrotestosterone (DHT). The estrogenic effects of clomiphene are secondary to the primary effects on HPTA function. Clomiphene exhibits no androgenic, anti-androgenic, or progestational effects, nor does it affect pituitary-thyroid or pituitary-adrenal function. In some clinical situations clomiphene citrate will produce negative feedback inhibition on The HPTA. This can usually be determined by clinical signs and laboratory profile.

Secondary hypogonadism is more common than primary gonadal failure and is seen in chronic and acute illnesses. Although testosterone has a role in erections, its importance in erectile dysfunction (ED) has been controversial. Hypogonadism produced by functional suppression of pituitary gonadotropins has been shown to correct with clomiphene citrate in a % of patients, but with a modest effect on sexual function.

It does appear that many men may have functional suppression of the central component of their hypothalamic–pituitary–testicular axis resulting from a variety of acute and chronic medical conditions and multiple drug use. The same is true for various types of anxiety.

Endurance Athlete:

Patients with an intact hypothalamic-pituitary-gonadal axis are most likely to respond to clomiphene citrate. To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism. Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period. Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being. Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with .tating hypogonadism related to endurance exercise.

Long Term AAS Use:

Tan, R.S. and D. Vasudevan, Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse. Fertil Steril, 2003. 79(1): p. 203-5.

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene.

DESIGN: Case report.

SETTING: University-affiliated andrology practice within family practice clinic.

PATIENT(S): A 30-year-old male.

INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months.

MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH.

RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis.

CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. The axis was previously shut off with multiple anabolic steroid abuse.

Multiple Causes:

A total of 178 men with secondary hypogonadism and ED received clomiphene citrate for 4 months. Sexual function improved in 75%, with no change in 25%, while significant increases in luteinizing hormone and free testosterone occurred in all patients.

It was found clinically that if the primary cause of the problem is corrected, clomiphene can occasionally be tapered and stopped, and the testosterone level will remain normal . In some patients the total treatment needs to be extended beyond 6 months. Quite frequently in men with ED and hypogonadism, correcting that the sexual problem may require additional methods of treatment. Nevertheless, correcting the testosterone deficit may have other beneficial effects. These may include increasing energy and well-being, as well as prevention of anemia or bone loss, depending on the severity of the hypogonadism. If patients cannot maintain their testosterone levels in the normal range after clomiphene is discontinued, permanent testosterone replacement with intramuscular injection, transdermal patches, or gels should be considered.

A minority, 39%, of the men will clinically respond to this treatment totally and this group will not have to consider artificial means of correcting their sexual dysfunction, or treatment of their comorbid medical or psychological factors. Decreased responses also occurred in men with diabetes, hypertension, coronary artery disease, and multiple medication use. Since these conditions are more prevalent with aging, chronic disease may be a more important determinant of sexual dysfunction. Men with anxiety-related disorders responded better to normalization of testosterone. Assessment of androgen status should be accomplished in all men with ED. For those with lower than normal age-matched levels of testosterone treatment directed at normalizing testosterone with clomiphene citrate is a viable alternative to giving androgen supplements.

Clomiphene citrate is generally well tolerated. Adverse reactions usually have been mild and transient and most have disappeared promptly after treatment has been discontinued. Visual Symptoms - Blurred vision, lights, floaters, waves, unspecified visual complaints, photophobia, diplopia, scotomata, phosphenes and headaches are those most common I have encountered. Reducing the dosage or discontinuing the medication resolves these side effects.

Clomiphene is administered orally and is well absorbed from the GI tract. Clomiphene is a combination of racemic isomers, enclomiphene and zuclomiphene, which may have different pharmacokinetic and pharmacodynamic parameters that have not been completely elucidated. Zuclomiphene is thought to be the more estrogenic isomer. The metabolic fate of clomiphene has not been completely established, but the drug appears to undergo hepatic metabolism. Both unchanged drug and its metabolites are excreted in the feces via the bile. Stereo-specific enterohepatic recycling or sequestering seems to occur also, with the zuclomiphene isomer accumulating over several cycles of treatment. However, even with continued cycles of use, combined maximum plasma levels of enclomiphene and zuclomiphene do not appear to exceed 100 mmol/L. The half-life of clomiphene is reported to be 5 days, but studies with radiolabeled doses have demonstrated that the drug may be found in the feces for up to 6 weeks.

sele137:
HCG timing and dosing for shut down recovery....logic behind it all by Michael C. Scally, M.D.
Q: What's the logic behind all the different timing and dosing of HCG ?? We hear taking it every day, every other day, every 3rd, 4th, or 5th day. What's the logic or science behind all the different timings? Shouldn't HCG timing mimic the bodies natural pulsing of LH? What is that exactly? Where do all you guys get the timing from? Articles, studies, colleagues?

What about the dosing ? I hear to take it easy to prevent desensitizing the testes. With this you hear anywhere from 100 units to 250 units to play it safe. Others say anywhere from 500 to 2500 units at a time...Isn't that a bit much ?

What about the length of time? I hear two clinics suggest 10 days; others say 3-5 weeks. Where does all this come from and who's right? Help me! Does anyone have any hard info here ?

A: Almost everything you hear or read will be anecdotal and therefore subject to no verification. Experiences with hCG while on TRT are posted. The use of hCG for PCT is only partly related to its use on TRT.

hCG while on TRT is used for two reasons. One reason is cosmetic. While on TRT it is not unusual and more often expected to have testicular atrophy. This is variable from individual to individual. The other reason is to act as a stimulus so the testicles do not shut down and therefore will be easier to initiate independent function after AAS cessation.

Desensitization is a potential problem with hCG. I do not think you will experience it with doses of 500IU or less 3X/week. Studies have used this dose for considerably long periods. In my patients when hCG was used while on AAS the dose was 1000IU every 3 days with one month on hCG followed by one month off hCG.

hCG for PCT involves additional concepts. This is the timing of hCG in relation to other medications for return of HPTA functionality. Under normal conditions the HPTA is a tightly coupled dynamic feedback loop. It is this coupling that has to be achieved after AAS cessation to return to normal. The analogy I use is the starting of a car by pushing it from behind. Alone the care will not start but with pushing the clutch can be popped and the car started.

After AAS cessation the secretion of LH is nil. It will not be able to initiate T production until a certain stimulus LH level is reached. Studies have shown that the time for this to occur can be lengthy. Thus the idea is to ‘push’ the testicles with hCG and get them started. Once T production is initiated the dependent variable is LH. If the hCG is withdrawn without adequate LH to couple with the testicles return of HPTA functionality will fail.

The increased production of LH is achieved by a dual action of clomiphene citrate and tamoxifen. Clomiphene is a mixed agonist/antagonist (SERM) at the estradiol receptor. Clomiphene will increase the secretion of LH by action at the hypothalamo-pituitary area. Clomiphene will cause an increase in LH and secondarily increases in T and estradiol. Estradiol has a negative feedback influence on the HPTA. Estradiol is 200X the inhibitory effect of T per molar basis. Normal serum levels are the following:

Testosterone: 3-10 ng/ml (10-35 nM/L)
Estradiol: 15-65 pg/ml (55-240 pmol/L)

Tamoxifen will counteract the effect of the estradiol. Once the hCG is withdrawn the LH, initiated by clomiphene and tamoxifen, will couple with the testicles and take over production of T by the testicles. The levels of LH to maintain and couple with the testicles are maintained by clomiphene and tamoxifen. Clomiphene is continued for 15 days while Tamoxifen is continued for 30 days.

In healthy adult men, circulating levels of testosterone have a distinct pattern, with increasing levels during sleep toward a maximum around the time of awakening and a decrease during the day. In PCT hCG is administered every other day. I suggest the same time each injection in an attempt to simulate this rhythm. This is purely empirical but I recommend hCG at bedtime (2200). Clomiphene is taken in divided doses of 50mg 2X/day.

sele137:
Why Use Both Clomid and Nolvadex Together by Michael C. Scally, M.D.
Q: I have read that Clomid and Novadex are very similar products. Is this true? If so why would you need to take both?

A: The administration of antiestrogens is a common treatment because anti estrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this  lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of antiestrogens on testicular spermatogenesis or steroidogenesis.

Clomiphene is a synthetic derivative an estrogen. Clomid is a mixed agonist/antagonist for the estradiol receptor. Tamoxifen is a pure estradiol receptor antagonist. Clomid acts as an estrogen, rather than an antiestrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level.

Perusal of the literature thus indicates that clomiphene acts in several ways in the human male; (a) due to its similarity of structure to stilbesterol it binds with receptor sites in the hypothalamus and pituitary, (b) It stimulates gonadotrophin secretion by acting on the hypothalamo-hypophyseal system, (c) the inhibitory effects of high levels of circulating estrogens (produced under the influence of clomiphene) on hypothalamo-hypophyseal axis are possibly prevented by its potent antiestrogenic behaviour. The result of these varied effects of clomiphene is an overall increase in gonadotrophin and estrogen secretion and accounts for their increase under clinical conditions.

In one study the administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels.

Cochran database summary showed ten studies involving 738 men were included. Five of the trials did not specify method of randomization. Antiestrogens had a positive effect on endocrinal outcomes, such as serum testosterone levels. Antiestrogens appear to have a beneficial effect on endocrinal outcomes, but there is not enough evidence to evaluate the use of antiestrogens for increasing the fertility of males with idiopathic oligo-asthenospermia.

In the over one-thousand patients I have treated for HPTA normalization after AAS cessation i have used the combination of clomiphene citrate and tamoxifen. I have used clomiphene citrate alone in many cases. I added tamoxifen to the protocol to see if I could get a better clinical response. This seemed to be the case although I have not had the opportunity to evaluate the data. When both compounds are used the clomiphene citrate is discontinued first and the tamoxifen is continued for 2 more weeks. as I stated in the post on hCG injections it is imperative to be tested while on the medications. thus one would be tested ~3-5 days before the tamoxifen expires. In the 1st stage described in the hCG post one tests for testosterone only. the serum T level determines whether or not the hCG is halted. In the typical situation the hCG is stopped and the CC & tamoxifen continued. the lab tests at the end of the oral meds is LH & T.

zzz:
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