estrogen levels pattern

[SilverTest]

hey guys,

when we do a cycle , and estrogen levels go up , after we stop the injections , do they stay up longer than the test or do they go down as the test go down , so at the end of the cycle we have :

1- low test and low estro ??

2- low test and high estro ??

[Swifto]

hey guys,

when we do a cycle , and estrogen levels go up , after we stop the injections , do they stay up longer than the test or do they go down as the test go down , so at the end of the cycle we have :

1- low test and low estro ??

2- low test and high estro ??

Usually, high Test = High estrogen and low Test = low estrogen. But there are exceptions. Such as obese or severly overweight people (or fat ****s).

They have high estrogen levels due to high adipose tissue and low testosterone. The body senses a high estrogen level and thinks its because of elevated testosterone output, then reduces serum T. See the cycle?

Estrogen, is primarily produced via aromoatse from testosterone (around 70%). But other sources are adipose tissue, bones, brain, testis, skin. and adrenal cortex.

Elevated estrogen has been linked to bad lipids, acne, gyno, water retention, heart disease, elevated BP, cancer's etc...

[Swifto]

During PCT we have low estrogen levels due to low aromotasation of testosterone. Therefore, AI's shouldnt be used IMHO. Unless your PCT protocol uses HCG.

Why reduce estrogen further when its already low and risk lowering estrogen too much, which has its own side effects. Loss of labido, bad lipids, CNS function etc...

[SilverTest]

damn swifto i swear i was waiting for you to reply haha .

great answer man thanks.

[Swifto]

damn swifto i swear i was waiting for you to reply haha .

great answer man thanks.

Estrogen really shouldnt be in high ranges in males IMHO. For the reasons stated above.

The Eestrogen Receptor (ER) will also directly inhibit LH and FSH production at the pituitary. Not solely through acitivty at the hypothalamus. It will also directly inhibit leydig cell function, thus testosterone output at the testis. It will do this by limiting leydig cell population, or estradiol (E2)-induced inhibition of enzyme activity.


The potential roles of estrogens in regulating Leydig cell development and function:


Tom O. Abney, , a

a Department of Physiology and Endocrinology, Medical College of Georgia, Augusta, Georgia 30912, USA


Available online 10 September 1999.

Abstract
It is generally agreed that estrogens, principally estradiol-17β, are synthesized by and act in the testis of mammals, including humans. The site of estradiol synthesis in the testis is generally believed to begin in the Sertoli cell and switch to the Leydig cell during neonatal development where a gonadotropin-regulated aromatase is present. Numerous studies suggest that the primary target cell of estradiol in the testis at all ages is the Leydig cell. In fact, the Leydig cell is known to possess an estrogen receptor that binds estradiol in the classic manner. The mechanism of estradiol action and the role of its receptor in the testis, however, remain unresolved. In Leydig cells, estradiol appears to induce several alterations that are dependent in large part on the developmental stage of the Leydig cell. In the fetal and neonatal testes, estradiol appears to block the ontogenic development of Leydig cells from precursor cells. There is also evidence that estradiol similarly blocks the regeneration of Leydig cells in the testis of mature, ethane dimethylsulfonate-treated animals. Evidence indicates that the precursor cell possesses high levels of estrogen receptors relative to that of the Leydig cell. It is postulated that estradiol is a paracrine factor involved in regulating the interstitial population of Leydig cells. Evidence also indicates that estradiol acts directly in the mature testis to block androgen production. It appears to do so by inhibiting the activities of several steroidogenic enzymes involved in testosterone synthesis. Although the more conventional receptor-mediated mode of action is feasible, several studies have suggested that this action might entail direct competitive inhibition of key steroidogenic enzymes by estradiol. In summary, the net biologic effect of estradiol in the testis appears to be inhibition of androgen production, either by limiting development and growth of the Leydig cell population or through direct action in the Leydig cell.

[Swifto]

I'm glad I could be of some help.

Using an AI when obese will help increase testosterone production. I had this debate recently with that twat Pinnacle/RR/Bobby.