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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Testosterone (DHT) and Prostate Enlargement
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<blockquote data-quote="madman" data-source="post: 124321" data-attributes="member: 13851"><p>Why are you so dead set on" Its the DHT."</p><p></p><p>Much more is involved than just DHT.</p><p></p><p><strong>Epidemology and risk factors of lower urinary tract symptoms/benign prostatic hyperplasia and erectile dysfunction</strong></p><p></p><p>The role of androgens in determining LUTS/BPH and the physiopathological ways that may lead to it are still a matter of debate. Although an increased androgen signaling is clearly implicated in the first two waves of prostate growth (the first one at birth, the second one at puberty – under the influence of increasing testosterone levels), its role in the third phase (starting at mid-late adulthood and involving selectively the periurethral zone), is not completely clear yet. In fact, a clear dose–response relationship between circulating androgen levels and BPH has never been demonstrated. In addition, during male senescence, androgens tend to decrease and not to increase. Several recent studies indicate that a low testosterone, more than a high one, might have a detrimental effect on prostate biology. In fact, LUTS can even be lessened by androgen supplementation in hypogonadal men [65].</p><p></p><p>Recent data indicate that not only low testosterone but also high estradiol can favor BPH/LUTS progression. It is important to note that circulating testosterone is actively metabolized to estrogens and part of testosterone hormonal activity depends upon its binding to the estrogen receptors (ERs) that are present in both the prostate and bladder. In addition, the enzyme P450 aromatase that converts androgens to estrogens is highly expressed not only in fat tissue but also in the urogenital tract. Marmorston et al. showed an increased estrogen/androgen ratio almost half a century ago [66] reporting that the estrogen/androgen ratio in 24-h urinary collections was elevated in men with BPH, as compared to normal controls. Many studies have reported a correlation between plasma 17b-estradiol levels and prostate volume or other features of LUTS/BPH, while others have not. The fear of clinicians to start a TRT on hypogonadal men with LUTS/ BPH must be redefined based on this upcoming evidence [65]. It is necessary to establish ways to determine which patients with LUTS/BPH, and even combined phenotype LUTS/BPH – ED, may benefit from TRT and in which terms; for this purpose, more studies are needed [61].</p></blockquote><p></p>
[QUOTE="madman, post: 124321, member: 13851"] Why are you so dead set on" Its the DHT." Much more is involved than just DHT. [B]Epidemology and risk factors of lower urinary tract symptoms/benign prostatic hyperplasia and erectile dysfunction[/B] The role of androgens in determining LUTS/BPH and the physiopathological ways that may lead to it are still a matter of debate. Although an increased androgen signaling is clearly implicated in the first two waves of prostate growth (the first one at birth, the second one at puberty – under the influence of increasing testosterone levels), its role in the third phase (starting at mid-late adulthood and involving selectively the periurethral zone), is not completely clear yet. In fact, a clear dose–response relationship between circulating androgen levels and BPH has never been demonstrated. In addition, during male senescence, androgens tend to decrease and not to increase. Several recent studies indicate that a low testosterone, more than a high one, might have a detrimental effect on prostate biology. In fact, LUTS can even be lessened by androgen supplementation in hypogonadal men [65]. Recent data indicate that not only low testosterone but also high estradiol can favor BPH/LUTS progression. It is important to note that circulating testosterone is actively metabolized to estrogens and part of testosterone hormonal activity depends upon its binding to the estrogen receptors (ERs) that are present in both the prostate and bladder. In addition, the enzyme P450 aromatase that converts androgens to estrogens is highly expressed not only in fat tissue but also in the urogenital tract. Marmorston et al. showed an increased estrogen/androgen ratio almost half a century ago [66] reporting that the estrogen/androgen ratio in 24-h urinary collections was elevated in men with BPH, as compared to normal controls. Many studies have reported a correlation between plasma 17b-estradiol levels and prostate volume or other features of LUTS/BPH, while others have not. The fear of clinicians to start a TRT on hypogonadal men with LUTS/ BPH must be redefined based on this upcoming evidence [65]. It is necessary to establish ways to determine which patients with LUTS/BPH, and even combined phenotype LUTS/BPH – ED, may benefit from TRT and in which terms; for this purpose, more studies are needed [61]. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Testosterone (DHT) and Prostate Enlargement
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