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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
Physiology of Erection and Erectile Dysfunction
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<blockquote data-quote="madman" data-source="post: 216010" data-attributes="member: 13851"><p><em><strong>*ED often is the end result of multiple pathophysiologic processes</strong></em></p><p></p><p><strong>*<em><u>Arteriogenic ED, which accounts for a majority of cases, has been strongly linked to the following conditions</u>: </em></strong><em><strong>hypertension, hyperlipidemia, tobacco use, metabolic syndrome/obesity, sedentary lifestyle, diabetes, and pelvic radiation.33–38 Doppler ultrasound has been used to correlate decreased peak systolic velocity of the cavernosal arteries with underlying vascular disease and risk of cardiovascular events.39,40</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*<em><strong>The pathologic mechanism underlying arteriogenic ED is likely multifactorial, including 1 or more of the following, as suggested by Musicki and colleagues41 in a 2015 review: (1) endothelial dysfunction, (2) smooth muscle alterations, (3) autonomic dysregulation (discussed later), (4) hypogonadism (see endocrine section), and (5) metabolic defects</strong></em></strong></em></p><p><em><strong><em><strong></strong></em></strong></em></p><p><em><strong><em><strong><em><strong>*Alterations of vascular smooth muscle content and function have been suggested as contributing factors to ED</strong></em></strong></em></strong></em></p><p><em><strong></strong></em></p><p><em><strong>*There is a complex relationship between ED and serum testosterone levels</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*<em><strong>Further support for the androgen-dependent extent of erectile function includes a <u>threshold testosterone value of 200 ng/dL for regular nocturnal erections</u></strong></em></strong></em></p><p><em><strong><em><strong><u></u></strong></em></strong></em></p><p><em><strong><em><strong><u><em><strong>*Studies have demonstrated that testosterone and DHT stimulate nNOS gene expression and increase NO in the corpora during erections.72,74 Van den Broeck and colleagues75 confirmed dose-dependent relaxation of human corpora cavernosal tissue with increasing testosterone and DHT</strong></em></u></strong></em></strong></em></p><p><em><strong></strong></em></p><p><em><strong>*Hyperprolactinemia results in reproductive as well as sexual dysfunction. Symptoms associated with hyperprolactinemia include loss of libido, ED, galactorrhea, gynecomastia, and infertility. <u>These symptoms typically occur only at severely elevated levels (>35 ng/mL or 735 mU/L)</u>.76</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*Hyperthyroidism or hypothyroidism also may be associated with ED.</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*A direct effect of thyroxine may also be at play in thyroid hormone ED because both alpha and beta thyroxine receptors have been shown to be present in endothelial and smooth muscle cells from human corpora cavernosa.82</strong></em></p><p></p><p><strong><em>*Pscyhogenic ED may not be a primary etiology in most cases but it is a contributing factor in virtually all cases</em></strong></p><p></p><p><em><strong>*The degree to which ED is psychogenic versus physiologic is difficult to parse out; isolated psychogenic ED is considered a diagnosis of exclusion clinically.</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 216010, member: 13851"] [I][B]*ED often is the end result of multiple pathophysiologic processes[/B][/I] [B]*[I][U]Arteriogenic ED, which accounts for a majority of cases, has been strongly linked to the following conditions[/U]: [/I][/B][I][B]hypertension, hyperlipidemia, tobacco use, metabolic syndrome/obesity, sedentary lifestyle, diabetes, and pelvic radiation.33–38 Doppler ultrasound has been used to correlate decreased peak systolic velocity of the cavernosal arteries with underlying vascular disease and risk of cardiovascular events.39,40 *[I][B]The pathologic mechanism underlying arteriogenic ED is likely multifactorial, including 1 or more of the following, as suggested by Musicki and colleagues41 in a 2015 review: (1) endothelial dysfunction, (2) smooth muscle alterations, (3) autonomic dysregulation (discussed later), (4) hypogonadism (see endocrine section), and (5) metabolic defects [I][B]*Alterations of vascular smooth muscle content and function have been suggested as contributing factors to ED[/B][/I][/B][/I] *There is a complex relationship between ED and serum testosterone levels *[I][B]Further support for the androgen-dependent extent of erectile function includes a [U]threshold testosterone value of 200 ng/dL for regular nocturnal erections [I][B]*Studies have demonstrated that testosterone and DHT stimulate nNOS gene expression and increase NO in the corpora during erections.72,74 Van den Broeck and colleagues75 confirmed dose-dependent relaxation of human corpora cavernosal tissue with increasing testosterone and DHT[/B][/I][/U][/B][/I] *Hyperprolactinemia results in reproductive as well as sexual dysfunction. Symptoms associated with hyperprolactinemia include loss of libido, ED, galactorrhea, gynecomastia, and infertility. [U]These symptoms typically occur only at severely elevated levels (>35 ng/mL or 735 mU/L)[/U].76 *Hyperthyroidism or hypothyroidism also may be associated with ED. *A direct effect of thyroxine may also be at play in thyroid hormone ED because both alpha and beta thyroxine receptors have been shown to be present in endothelial and smooth muscle cells from human corpora cavernosa.82[/B][/I] [B][I]*Pscyhogenic ED may not be a primary etiology in most cases but it is a contributing factor in virtually all cases[/I][/B] [I][B]*The degree to which ED is psychogenic versus physiologic is difficult to parse out; isolated psychogenic ED is considered a diagnosis of exclusion clinically.[/B][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
Physiology of Erection and Erectile Dysfunction
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