Nolva question

[jmcbride69]

Ok I have my clomid ready for pct and don't think I'm gonna run hcg pct as I will be running it during cycle. I keep seeing a lot of people having nolva along with clomid. Is this a must or am I good with the clomid.

500 mg test wk
12.5 mg aromasin Ed on cycle
500 ius hcg twice a well the day before test

[OdinsOtherSon]

Might want to consider changing your hcg protocol to 250iu twice per week (day prior to test) as well as adding nolva. You are planning to break your test up into two pins instead of one 500mg pin, right? Read MickeyKnox's thread about setting up first cycles. It should have been pretty close to the top of this page. Sounds like you may need to stop, and do some more detailed research. My $0.02

http://forums.steroid.com/showthread...cles-Look-here

[jmcbride69]

Yes of course 250mgs of test e twice a week and 250 iu of hcg the day before each pin. Yes I have talked to mickeyknox and have read the beginners forum. He's the one who got me down to 250iu twice a week the day before. I was gonna do it the day after.

I'm just trying to figure out if nolva is a must or am I good running clomid pct without the nolva. I really do appreciate everybody's input though. Love this place

[OdinsOtherSon]

Well, I know that some folks here are GTG using Nolva as stand alone PCT with a test only cycle BUT I'm not suggesting it. Its person dependent. My personal opinion is, add nolva. If you just want to run one PCT product, I'd personally use Nolva in place of clomid. Here is another good thread on PCT. LOTS of good info here. Good luck bro!

http://forums.steroid.com/showthread...ed-08-12-09%29

[MickeyKnox]

Run a standard PCT just the ones set up in the Beginners Cycle thread.

Clomid 75/50/50/50 *If you're using tablets, first wk can be 100mg.
Nolva 40/20/20/20


From my friend 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 [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.

Its a long read but I bolded the most pertinent portion. IMO this explains why it’s most prudent to use both in our pct protocols. I posted it because often we see the question cant i just use nolvadex? This shows the importance of the addition of clomid as well. Contrary to popular belief they aren’t the same but nolvadex is just stronger.

This excerpt from an interview with Dr Scally probably explains it better - makes a lot of sense.

"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

[jmcbride69]

Thanks a lot Micky. I'm gonna go ahead and get me some nolva. I've got plenty of time till pct. man I thought I did my research for the most part but I guess I was wrong