Ball Shrinkage - HPTA - Anti-Estrogen and fun stuff like that...

Hello...welcome to my thread...fellow ARers... :D

Well, it has been a while since I've studied the HPTA to a great extent. I, of course, look at the main points here and there, due to an interest in AAS.

I'm wondering, to what extent does anti-e meds like Nolvadex help with sides like testicular atrophy during a (any) cycle? When the hypothalamus detects a significant amount of estrogen, it normally will not help to produce hormones such as testosterone. Consequently, testicular atrophy (ball shrinkage) can occur.

So, to what extent do you think 20mg of Nolvadex per day plays a role in protecting one from testicular atrophy during an AAS cycle?

I'm directing this towards the affects of Nolvadex on testicular atrophy, regardless of the individual user or type of cycle.

Thanks for your input.

RA

during a cycle nolva really wont help maintain testicualr function. because as long as there is an exergoneous source of testosterone, u natural output will decrease one way or another. 20 mg of nolva during a cycle is insane unless u get gyno. imho nolva during a cycle is insane. if u wanna keep water off and prevent gyno, get some liquidex. IT HAS BEEN PROVEN THAT NOLVA DECREASES IGF-1 SERUM LEVELS.

why do people want to use nolva so bad, just use some l-dex to keep water off. it will also decrease the likelyhood of getting gyno.

here is the proof:

--------------------------------taken from a university study-----------------
Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men

--------------------------------end------------------------------------------

cheers !