anterior pituitary desensitization from serms (Theory)

[Nike3844]

I'm new to the forum and wanted to bring my thoughts to the table to see what the knowledgeable members on this board thought.

My theory: The increase of LH/FSH from high doses of serms, will cause desensitization of the anterior pituitary, thus causing elongated recovery.

The reason I have come up with this theory is because from my personal experience, I believe I have encountered this multiple times. After one of my PH cycles years ago, I took Nolva (40/40/20/10) for my pct with some otc ai's and test boosters. I had blood taken about 2 weeks into the nolva and it was something like total test 1028, e2 48, LH 17. When i came off of it after about 4 months I got blood taken again because I was still experiencing ED, and low libido. My results were total test 410, e2 20, LH 1.8. So there was obviously a problem with my pituitary. After about 10 months of ending my pct, my libido and ED corrected itself and everything was perfectly normal. The only problem is I didnt get blood taken to see what my baseline levels actually were. But what I think happened is the high dose of nolva overstimulated my pituitary which caused it to take a while to work again. I have read studies that serms can do this, so if this were the case, how would you go about dosing the serm next time? How could I make the transition smoother so that I would next experience secondary hypogonadism next time, and hopefully not for good?

edit: I have used nolva and clomid..

stats:
age:22
years training: 6
height- 6'0
weight 225

EDUCATED thoughts and comments appreciated,
Thanks

 

[Nike3844]

Heres a study i found that kind of supports increased gnrh to the anterior pituitary will desensitize the cells in the pituitary itself.

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro

E. Y. Adashi, A. J. Hsueh, T. H. Bambino and S. S. Yen

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

In Summary: These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex , pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.

 

[stevesmi]

Nelson is the guy who would be interested in discussing this.

here on elite we shy away from the clomid/nolva pct for this very reason. you did not end up recovering correctly. the pct you will see the experienced guys on here do are totally different than other sites but i have noticed even other sites are now copying it.

proper ancillaries during
hcg/hmg to blast before pct
very small dose clomid 12-25 per day tops along with natty supps and DAA.

most of us on here never recommend nolva at all

 

[Nike3844]

Ah good to know... I've been out of the loop for a while. That pct protocol sounds like it would be a lot more effective. Do you recommend hcg throughout the whole cycle versus blasting at the end? Also what would be the point of HMG while on, unless you are trying to have a kid? Does FSH supplementation with HMG augment preserving testicular function as well?

Thanks,