Do you need both?

[brianlb98]

nolvadex and clomid, are they both necessary for a pcr?

It would be first cycle with test-c only, for twelve weeks.

[jimmyinkedup]

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 LH secretion [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 repla***ent 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 repla***ent 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”) isthe 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 cis (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. Enclomiphene alone might be a good candidate to restore HPTA function.

The bottom line - its prob a good idea to use both (see bold)

[songdog]

Doing a lil research prior to a cycle is a good thing.