ExcelMale
Menu
Home
What's new
Latest activity
Forums
New posts
Search forums
What's new
New posts
Latest activity
Videos
Lab Tests
Doctor Finder
Buy Books
About Us
Men’s Health Coaching
Log in
Register
What's new
Search
Search
Search titles only
By:
New posts
Search forums
Menu
Log in
Register
Navigation
Install the app
Install
More options
Contact us
Close Menu
Forums
Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
An overview of leading pathophysiologic theories in BPH - Androgens and estrogens
JavaScript is disabled. For a better experience, please enable JavaScript in your browser before proceeding.
You are using an out of date browser. It may not display this or other websites correctly.
You should upgrade or use an
alternative browser
.
Reply to thread
Message
<blockquote data-quote="madman" data-source="post: 276627" data-attributes="member: 13851"><p>Androgen is required to prevent atrophy of the gland.</p><p></p><p></p><p><em><strong>*Normal prostate glands undergo atrophy when serum androgens are greatly reduced via castration or administration of LHRH agonists</strong></em></p><p></p><p></p><p></p><p></p><p><strong>Testosterone and Prostate Cancer</strong></p><p></p><p><em><strong>It is widely recognized that the presence of <u>adequate serum levels of testosterone</u> is necessary for the development of the prostate. Testosterone (T) can act <u>directly on androgen receptors to exert their action or can be converted by 5-alpha-reductase into dihydrotestosterone (DHT) or to estradiol by the aromatase enzyme complex</u> [1].</strong></em></p><p><em></em></p><p><em>There are several reasons why it appears logical to believe that testosterone therapy may stimulate prostate cancer. <strong>The prostate does not <u>develop properly without androgen stimulation</u>.</strong> <strong>Normal prostate glands undergo <u>atrophy when serum androgens are greatly reduced via castration or administration of LHRH agonists</u>. </strong>Furthermore, most prostate cancers are dependent on androgens in the early stages of progression and demonstrate regression with androgen ablation. Consequently, the presence of excessive androgenic stimulation as an etiologic factor in prostate carcinogenesis appears logical [1–5].</em></p><p><em></em></p><p><em>However, a number of studies have suggested that testosterone administration in supraphysiological doses to healthy men did not result in a significant increase in prostate-specific antigen (PSA), nor prostate volume or urinary symptoms [6, 7].PSA also does not seem to be influenced by the circadian rhythm of testosterone levels [8].</em></p><p><em></em></p><p><em>A variety of studies in PCa, including experiments in animals, cell lines, and humans, indicate that prostate tissue (benign or malignant) responds quickly and vigorously to the addition of testosterone when it is in an androgen-deprived state. However, at higher concentrations, prostate tissue becomes unresponsive to this hormone [9].</em></p></blockquote><p></p>
[QUOTE="madman, post: 276627, member: 13851"] Androgen is required to prevent atrophy of the gland. [I][B]*Normal prostate glands undergo atrophy when serum androgens are greatly reduced via castration or administration of LHRH agonists[/B][/I] [B]Testosterone and Prostate Cancer[/B] [I][B]It is widely recognized that the presence of [U]adequate serum levels of testosterone[/U] is necessary for the development of the prostate. Testosterone (T) can act [U]directly on androgen receptors to exert their action or can be converted by 5-alpha-reductase into dihydrotestosterone (DHT) or to estradiol by the aromatase enzyme complex[/U] [1].[/B] There are several reasons why it appears logical to believe that testosterone therapy may stimulate prostate cancer. [B]The prostate does not [U]develop properly without androgen stimulation[/U].[/B] [B]Normal prostate glands undergo [U]atrophy when serum androgens are greatly reduced via castration or administration of LHRH agonists[/U]. [/B]Furthermore, most prostate cancers are dependent on androgens in the early stages of progression and demonstrate regression with androgen ablation. Consequently, the presence of excessive androgenic stimulation as an etiologic factor in prostate carcinogenesis appears logical [1–5]. However, a number of studies have suggested that testosterone administration in supraphysiological doses to healthy men did not result in a significant increase in prostate-specific antigen (PSA), nor prostate volume or urinary symptoms [6, 7].PSA also does not seem to be influenced by the circadian rhythm of testosterone levels [8]. A variety of studies in PCa, including experiments in animals, cell lines, and humans, indicate that prostate tissue (benign or malignant) responds quickly and vigorously to the addition of testosterone when it is in an androgen-deprived state. However, at higher concentrations, prostate tissue becomes unresponsive to this hormone [9].[/I] [/QUOTE]
Insert quotes…
Verification
Post reply
Share this page
Facebook
X (Twitter)
Reddit
Pinterest
Tumblr
WhatsApp
Email
Share
Link
Sponsors
Forums
Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
An overview of leading pathophysiologic theories in BPH - Androgens and estrogens
This site uses cookies to help personalise content, tailor your experience and to keep you logged in if you register.
By continuing to use this site, you are consenting to our use of cookies.
Accept
Learn more…
Top