"Clomid" a thing of the past?

[Stosh_112]

Been reading that clomid is being phased out by Nolva only for pct. I know both hit diff receptors for htpa. Last year at this time it was Clomid100,100,50,50 Nolva 40,40,20,20. Now a days its more like this Clomid 75,50,25,25 Nolva 40,40,20,20,20 with the extra wk of nolva. Just wanted to get some feedback on the present PCT...

[Gaspaco]

A lot of guys get bit-chy moods and depressions with clomid, you got to try and see which PCT works for you best.

[Stosh_112]

Yea i taper my clomid from 100mg for 3-4 days just to frontload and get a quicker responce. Then run an even 50 for 3 wks. No problems. But i do like the idea of running Nolva an extra week.

[OdinsOtherSon]

Great post Stosh. I've been wondering about this myself. I think clomid is still a viable and useful compound that we should be using but perhaps not dosed nearly as high as it has historically been used. My approach to any compound is the same as the vets/mods take over in the hrt forum, "use the minimum amount for the desired effect," or as my wife likes to say when it comes to cooking and the number of ingredients you use, "less is more."

I'm probably gonna take a little heat for saying this, but oh well. I haven't personally practice this but have heard some positive things from this protocol. Granted, I'm moving away from your original premise here but it still speaks to the effective of nolva. I've heard of some substituting an AI on cycle for a protocol of 10mg of nolva instead.

Also in regards to PCT, I've read here of some guys using a nolva/torem protocol instead of nolva/clomid. Granted, torem is very, very similar to nolva (I think nolva is a 1st generation serm and torme is basically it's 2nd generation counterpart??)

[redz]

I still use clomid but I start at 50mg ed for 2 weeks then 25mg ed for 2 weeks along side Nolva.

[OdinsOtherSon]

redz, how do you dose your nolva and for how long? Thanks man.

[MickeyKnox]

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

[Stosh_112]

^^^^ Thanks Mickey! I'll be keeping clomid in the PCT mix. Just keep the dosage moderate to min.

[redz]

I use nova at 40mg Ed for 2 weeks then 20mg for 2 more

[RyanGreg]

So it would be better to dose clomid 50/50/25/25?

[MickeyKnox]

So it would be better to dose clomid 50/50/25/25?

Typically, you dont really need a lot of Clomid for PCT. This is one of those compounds where a little goes a long way. And personally, anything above 100mg for me impairs my vision - yellowish haze and somewhat blurry. Nothing extreme for some people, but it's certainly enough to cause me concern.

[Granovich]

my personal experience clomid didnt do anything.... only nolva works good for me... torem as well but clomid NOTHING even at 150mg Daily