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Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
Is DHT the Cause of BPH ( Prostate Enlargement ) or is it Estradiol?
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<blockquote data-quote="Nelson Vergel" data-source="post: 79002" data-attributes="member: 3"><p>Excellent question!</p><p></p><p></p><p>H<a href="https://academic.oup.com/edrv/article/38/3/220/3788611/Dihydrotestosterone-Biochemistry-Physiology-and" target="_blank">ere is the best DHT review paper out there.</a></p><p></p><p>Some quotes</p><p></p><p></p><p><span style="font-size: 15px">"<span style="color: #2A2A2A">Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not correlate with those found in androgen sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis."</span></span></p><p><span style="font-size: 15px"><span style="color: #2A2A2A"></span></span></p><p><span style="font-size: 15px"><span style="color: #2A2A2A">"The clinical benefits associated with lowered serum DHT levels after 5AR-Is appear to have led to the misconception that circulating DHT is an important stimulus for androgenic action in the prostate gland. However, studies in which serum DHT concentrations were markedly elevated by exogenous administration of DHT had almost no effect on prostate DHT concentrations, prostate size, and lower urinary tract symptoms (see “Intraprostatic Control Of DHT in the Presence of Fluctuating Levels of Circulating Androgens” and associated references). The reason for this highlights fundamentally important control mechanisms in androgen target tissues that finely regulate pathways for androgen synthesis and degradation to maintain DHT homeostasis. These intracellular processes do not appear to be affected by circulating DHT concentrations. Furthermore, it is well documented that DHT can be synthesized in androgen-sensitive tissues such as prostate from substrates other than T (</span><em>e.g.</em><span style="color: #2A2A2A">, from 17-hydroxypregnenolone and 17-hydroxyprogesterone in what is termed the “backdoor” pathway and from 5</span><em>&#945;</em><span style="color: #2A2A2A">-androstane-3</span><em>&#945;</em><span style="color: #2A2A2A">, 17-</span><em>&#946;</em><span style="color: #2A2A2A">-diol via the intracrine reverse synthesis pathway) (</span>4<span style="color: #2A2A2A">). We will also explore the implications of modest increases in serum DHT that are seen with T replacement therapy (TRT; including, for completeness, DHT preparations) for male hypogonadism and discuss why these likely have minimal clinical implications for men treated with androgens."</span></span></p><p></p><p><span style="font-size: 12px"><span style="color: #2A2A2A"><a href="https://academic.oup.com/edrv/article/38/3/220/3788611/Dihydrotestosterone-Biochemistry-Physiology-and" target="_blank">Source</a></span></span></p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 79002, member: 3"] Excellent question! H[URL='https://academic.oup.com/edrv/article/38/3/220/3788611/Dihydrotestosterone-Biochemistry-Physiology-and']ere is the best DHT review paper out there.[/URL] Some quotes [SIZE=15px]"[COLOR=#2A2A2A]Circulating levels of DHT in response to testosterone replacement therapy (TRT) do not correlate with those found in androgen sensitive tissue (e.g., prostate, adipose, muscle) due to local regulatory mechanisms that tightly control intracellular androgen homeostasis." "The clinical benefits associated with lowered serum DHT levels after 5AR-Is appear to have led to the misconception that circulating DHT is an important stimulus for androgenic action in the prostate gland. However, studies in which serum DHT concentrations were markedly elevated by exogenous administration of DHT had almost no effect on prostate DHT concentrations, prostate size, and lower urinary tract symptoms (see “Intraprostatic Control Of DHT in the Presence of Fluctuating Levels of Circulating Androgens” and associated references). The reason for this highlights fundamentally important control mechanisms in androgen target tissues that finely regulate pathways for androgen synthesis and degradation to maintain DHT homeostasis. These intracellular processes do not appear to be affected by circulating DHT concentrations. Furthermore, it is well documented that DHT can be synthesized in androgen-sensitive tissues such as prostate from substrates other than T ([/COLOR][I]e.g.[/I][COLOR=#2A2A2A], from 17-hydroxypregnenolone and 17-hydroxyprogesterone in what is termed the “backdoor” pathway and from 5[/COLOR][I]α[/I][COLOR=#2A2A2A]-androstane-3[/COLOR][I]α[/I][COLOR=#2A2A2A], 17-[/COLOR][I]β[/I][COLOR=#2A2A2A]-diol via the intracrine reverse synthesis pathway) ([/COLOR]4[COLOR=#2A2A2A]). We will also explore the implications of modest increases in serum DHT that are seen with T replacement therapy (TRT; including, for completeness, DHT preparations) for male hypogonadism and discuss why these likely have minimal clinical implications for men treated with androgens."[/COLOR][/SIZE] [SIZE=12px][COLOR=#2A2A2A][URL='https://academic.oup.com/edrv/article/38/3/220/3788611/Dihydrotestosterone-Biochemistry-Physiology-and']Source[/URL][/COLOR][/SIZE] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
Is DHT the Cause of BPH ( Prostate Enlargement ) or is it Estradiol?
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