Nolva vs Clomid.

[craig1414]

The above represents a solid SERM plan for most PCT plans; again, you do not need both Clomid and Nolvadex , we have simply laid out the dosing protocol for both; you simply need to pick one.


^ This was taken from the home page of our forum. All the research I have done and all the advice I have used for AAS, has always suggested using clomid AND nolva. So why is it that our own forum has different opinions? I understand these can be pretty harsh compounds. So who to believe? I am sure this has been discussed. I would just like some opinions. I am currently at 4 weeks of my 12 week cycle.
Test enanthate 250 mg 2x weekly Monday and Thursday.
0.25 arimidex eod.
Original plans are clomid and nolva for pct at usual dosage ( I have both on hand )
Basically my point is, is it necessary to use both? Some say no some say yes. Would love to get this settled, reminder that I am on a test e only cycle, soon to be adding anavar . Pretty mild in my opinion.
Appreciate it guys!

[Bigherm21]

You don't need both but what's the main purpose of pct? To recover so why risk it. Run both but some guys prefer clomid over nolva for nolva lowers igf. If that's the case and you're worried about it you can get igf. I've always ran both with aromasin and usually blast with hcg . Has always worked great for me. With the prices of serms and availability you should just run both. Both are very similar but are different.

[craig1414]

You don't need both but what's the main purpose of pct? To recover so why risk it. Run both but some guys prefer clomid over nolva for nolva lowers igf. If that's the case and you're worried about it you can get igf. I've always ran both with aromasin and usually blast with hcg. Has always worked great for me.

Makes sense. Just weird to do so much research and listen to so much advice and then see something different. I'm very paranoid about doing everything the best way possible as I'm sure you are as well. Thanks for your opinion

[Bigherm21]

Yep no problem. Just remember in the field you will get a million different opinions. It works how you do it and what works best for you because we're all different. Read up on dr scallys pct protocol. He's a dr and you can learn alot from him.

[MickeyKnox]

Originally posted by JimmyInk'd.

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 [57–61].

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 commitmentto 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 bind¬ing 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 secondar¬ily gonadal sex hormones. " Dr Michael Scally