What PCT after my cycle?

[Toosje]

Hey guys,

My cycle consisted of 12 week Test E at 500mg/week and the last 5 weeks Hdrol at 75mg/day.

I was originally planning on running Nolva at 20mg for 5 weeks. But was considering stacking it with either clomid or torem. What do you think?

[Granovich]

run nolva for 5 weeks its ok .. but do 40mg for first 2 weeks then go 20mg for the remaining of weeks
also run clomid for 4-5 weeks as well.. go 100/100/50/50

u can use torem if you want instead of Clomid. i think torem is better but most guys here like clomid

[AnabolicDoc]

I wouldn't do the Hdrol and instead do a kick start with Anadrol or Dbol .

Second, I would do Nolva at 20mg ed for 5-6 weeks and Clomid the first two weeks at 50mg/day and then two more weeks at 25mg/day. Last week or two would be Nolva only at 20mg ed.

I don't think there is anything wrong with Granovich's recommendation. And I think it's very effective in fact but you will experience side effects.

It's just that the emotional disturbances caused by Nolva and Clomid can be difficult for many and that's why I recommend trying the lower dosages. Some ppl recommend even higher doses of Clomid for the first few days and I think this has its own merits as far as causing quicker results. See what works for you. If you can tolerate the higher doses then more power to you.

Some argue that more than 20mg of Nolva per day only increases sides. Atomini referenced some articles that support this in one of his threads.

For various reasons that I don't feel like getting into now (bc I don't have the time). I like a short hCG blast in the beginning. Most who recommend an hcg blast, recommend doing so before starting the SERMs. I think it could be done even initiating the SERMs and there are many experts that agree. Those against hCG blasts will cite leydig cell desensitization as there reason but I think the evidence of this is weak if at all supportive.

Granovich, how is the triptorelin looking for PCT? I ordered a 100mcg vial just to have on hand.

Sorry, I wrote this in a rush on my phone and there may be many typos. My apologies

[Toosje]

Thanks for the advices. The cycle is already coming to an end, so a kick start is not possible anymore
Where Im from nolva only is usually the standard protocol, Ill add clomid or torem thanks

btw Ive always heard that nolva at more than 20mg a day has absolutely no use?

[AnabolicDoc]

Thanks for the advices. The cycle is already coming to an end, so a kick start is not possible anymore
Where Im from nolva only is usually the standard protocol, Ill add clomid or torem thanks

btw Ive always heard that nolva at more than 20mg a day has absolutely no use?

Atomini has posted references supporting your statement about nolva. You can search for his thread on this topic to see his references our just check PubMed.

[AnabolicDoc]

Atomini has posted references supporting your statement about nolva. You can search for his thread on this topic to see his references our just check PubMed.

[kelkel]

I wouldn't do the Hdrol and instead do a kick start with Anadrol or Dbol .

Second, I would do Nolva at 20mg ed for 5-6 weeks and Clomid the first two weeks at 50mg/day and then two more weeks at 25mg/day. Last week or two would be Nolva only at 20mg ed.

I don't think there is anything wrong with Granovich's recommendation. And I think it's very effective in fact but you will experience side effects.

It's just that the emotional disturbances caused by Nolva and Clomid can be difficult for many and that's why I recommend trying the lower dosages. Some ppl recommend even higher doses of Clomid for the first few days and I think this has its own merits as far as causing quicker results. See what works for you. If you can tolerate the higher doses then more power to you.

Some argue that more than 20mg of Nolva per day only increases sides. Atomini referenced some articles that support this in one of his threads.

For various reasons that I don't feel like getting into now (bc I don't have the time). I like a short hCG blast in the beginning. Most who recommend an hcg blast, recommend doing so before starting the SERMs. I think it could be done even initiating the SERMs and there are many experts that agree. Those against hCG blasts will cite leydig cell desensitization as there reason but I think the evidence of this is weak if at all supportive.

Granovich, how is the triptorelin looking for PCT? I ordered a 100mcg vial just to have on hand.

Sorry, I wrote this in a rush on my phone and there may be many typos. My apologies

Referring to Scally right doc?

[MickeyKnox]

From Jimmyink'dUp.

"The following explains why it is prudent to use BOTH Nolvadex and Clomid together in your PCT. It is by Dr Scally - probably the foremost expert in the United States on this topic.

Med Hypotheses. 2009 Jun;72(6):723-8. Epub 2009 Feb 23.
Anabolic steroid -induced hypogonadism--towards a unified hypothesis of anabolic steroid action.
Tan RS, Scally MC.

Source
HPT/Axis Inc., 1660 Beaconshire Road, Houston, TX 77077, USA.

Abstract

Anabolic steroid-induced hypogonadism (ASIH) is the functional incompetence of the testes with subnormal or impaired production of testosterone and/or spermatozoa due to administration of androgens or anabolic steroids . Anabolic-androgenic steroid (AAS), both prescription and nonprescription, use is a cause of ASIH. Current AAS use includes prescribing for wasting associated conditions. Nonprescription AAS use is also believed to lead to AAS dependency or addiction. Together these two uses account for more than four million males taking AAS in one form or another for a limited duration. While both of these uses deal with the effects of AAS administration they do not account for the period after AAS cessation. The signs and symptoms of ASIH directly impact the observation of an increase in muscle mass and muscle strength from AAS administration and also reflect what is believed to demonstrate AAS dependency. More significantly, AAS prescribing after cessation adds the comorbid condition of hypogonadism to their already existing chronic illness. ASIH is critical towards any future planned use of AAS or similar compound to effect positive changes in muscle mass and muscle strength as well as an understanding for what has been termed anabolic steroid dependency. The further understanding and treatments that mitigate or prevent ASIH could contribute to androgen therapies for wasting associated diseases and stopping nonprescription AAS use. This paper proposes a unified hypothesis that the net effects for anabolic steroid administration must necessarily include the period after their cessation or ASIH.

PMID: 19231088 [PubMed - indexed for MEDLINE]

Future treatments:
A treatment goal of HPTA restoration will have its basis in the regulation and control of testosterone production. The HPTA has two components, both spermatogenesis and testosterone production.
In males, luteinizing hormone (LH) secretion by the pituitary positively stimulates testicular testosterone (T) production; follicle-stimulating hormone (FSH) stimulates testicular spermatozoa production. The pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates LH and FSH secretion. In general, absent FSH, there is no spermatozoa production; absent LH, there is no testosterone production. Regulation of the secretion of GnRH, FSH, and LH occurs partially by the negative feedback of testosterone and estradiol at the level of the hypothalamo-pituitary. Estradiol has a much larger, inhibitory effect than testosterone, being 200-fold more effective in suppressing LHsecretion.

In the case of ASIH, where the individual suffers from functional hypogonadism and the belief for eventual return of function, treatment is directed at HPTA restoration. A medical quandary for physicians presented with hypogonadal patients secondary to AAS administration is there is currently no FDA approved drug to restore
HPTA function. Standard treatment to this point has been testosterone replacement therapy (TRT), human chorionic gonadotropin (hCG ), conservative therapy (‘‘watchful waiting” or ‘‘do nothing”), or off-label prescribing of aromatase inhibitors or selective estrogen receptor modulators (SERM).

The primary drawback of testosterone replacement and hCG administration is that this therapy is infinite in nature. These treatments will remedy the signs and symptoms associated with hypogonadism, but do not alleviate the need for a life-long commitment to therapy. Further, administration serves to further HPTA suppression.

Conservative therapy (‘‘watchful waiting” or ‘‘do nothing”) is the probably worst case option as this does nothing to treat the patient with ASIH. Also, conservative therapy will have the undesirable result of the nonprescription AAS user to return to AAS use as a means to avoid ASIH signs and symptoms.

The aromatase inhibitors demonstrate the ability to cause an elevation of the gonadotropins and secondarily serum testosterone [62]. The administration of SERMs is a common treatment in attempts to restore the HPTA because they increase LH secretion from the pituitary that leads to increased local testosterone production
[63–67].

Guay has used clomiphene citrate as therapy for erection dysfunction and secondary hypogonadism. Patients received clomiphene citrate 50 mg per day for 4 months in an attempt to raise their testosterone level [68]. Clomiphene has been reported in a case study to reverse andropause secondary to anabolic–androgenic steroid use [69]. The patient received clomiphene citrate 50 mg twice per day in an attempt to raise his testosterone level. The patient when followed up after two months had a relapse, tiredness and loss of libido, after discontinuing clomiphene citrate. There are case study reports demonstrating the effectiveness of the combination of clomiphene and tamoxifen in HPTA restoration after stopping AAS administration [70–73]. Clomiphene is a mixture of the trans (enclomiphene) and is (zuclomiphene) enantiomers, which have opposite effects upon the estradiol receptor [74]. Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor.


"Clomiphene is an antiestrogen, which decreases the estrogen effect in the body. It has a dual effect by stimulating the hypothalamic pituitary area and it has an antiestrogenic effect, so that it decreases the effect of estrogen in the body. Tamoxifen is more of a strict antiestrogen; it decreases the effect of estrogen in the body, and potentiates the action of clomiphene. Tamoxifen and clomiphene citrate compete with estrogen for estrogen receptor binding sites, thus eliminating excess estrogen circulation at the level of the hypothalamus and pituitary, allowing gonadotropin production to resume. Administering them together produces an elevation of LH and secondary gonadal sex hormones. " Dr Michael Scally"

[AnabolicDoc]

Referring to Scally right doc?

Yes, in regards to the hcg blast. I read that Crisler disagrees regarding the hcg blast, however. I think arguments can be made for both sides but it basically comes down to whether or not you believe that the leydig cells desensitize when exposed to high doses of hcg and if short term high dose hcg will cause long term blunting of LH release.