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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
ED in Men on the Rise: Is There a Link with Endocrine Disrupting Chemicals?
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<blockquote data-quote="madman" data-source="post: 211201" data-attributes="member: 13851"><p><strong>Abstract</strong></p><p></p><p><em>Erectile dysfunction (ED) is one of the most prevalent chronic conditions affecting men. <strong>ED can arise from disruptions during development, affecting the patterning of erectile tissues in the penis and/or disruptions in adulthood that impact sexual stimuli, neural pathways, molecular changes, and endocrine signalling that are required to drive erection.</strong> Sexual stimulation activates the parasympathetic system which causes nerve terminals in the penis to release nitric oxide (NO). As a result, the penile blood vessels dilate, allowing the penis to engorge with blood. This expansion subsequently compresses the veins surrounding the erectile tissue, restricting venous outflow. As a result, the blood pressure localised in the penis increases dramatically to produce a rigid erection, a process known as tumescence. The sympathetic pathway releases noradrenaline (NA) which causes detumescence: the reversion of the penis to the flaccid state. <strong>Androgen signalling is critical for erectile function through its role in penis development and in regulating the physiological processes driving erection in the adult. Interestingly, estrogen signaling is also implicated in penis development and potentially in processes that regulate erectile function during adulthood. Given that endocrine signalling has a prominent role in erectile function, it is likely that exposure to endocrine-disrupting chemicals (EDCs) is a risk factor for ED, although this is an under-researched field.</strong> Thus, our review provides a detailed description of the underlying biology of erectile function with a focus on the role of endocrine signalling, exploring the potential link between EDCs and ED based on animal and human studies.</em></p><p></p><p></p><p></p><p></p><p><strong>Erectile Dysfunction</strong></p><p></p><p><em>Erectile Dysfunction Erectile Dysfunction (ED) is defined as the consistent or repeated inability to acquire or sustain an erection sufficient for satisfactory sexual performance [McCabe et al., 2016]. The 5-item International Index of Erectile Function (IIEF-5) self-questionnaire categorizes the severity of ED based on the numerical score (each of the 5 questions is worth 5 points) as no ED (22–25), mild (17–21), mild to moderate (12–16), moderate (8–11), or severe (1–7) [Rhoden et al., 2002]. <strong>The erectile function relies on a combination of organic (structural, neurologic, vascular, and endocrine) and psychogenic factors. Thus, ED can have a number of aetiologies that are broadly classified as either organic or psychogenic [Johannes et al., 2000]. <u>Psychogenic risk factors</u> for ED include depression and anxiety [Yang et al., 2019], although these are beyond the scope of this review. <u>Organic risk factors</u> include vascular, neurologic, and endocrine abnormalities [reviewed in Ludwig and Phillips, 2014].</strong> Interestingly, since the penile vascular tissue that is responsible for an erection is a component of the global vascular system, ED of vascular origin is often an indicator of systemic endothelial dysfunction [Virag et al., 1981]. Thus, ED not only disrupts the quality of life but can also be a strong indicator of cardiovascular disease [Gandaglia et al., 2014].</em></p><p></p><p></p><p><strong>Physiology of Erectile Function </strong></p><p><em>-Neural Stimulation</em></p><p><em></em></p><p><em>-Anatomy, Vasculature, and Hemodynamics of Erection</em></p><p><em>-Calcium-Mediated Penile Smooth Muscle Contraction/Relaxation and RhoA/Rho KinaseMediated Calcium Sensitisation</em></p><p><em>-Nitric Oxide (NO)-cGMP Mediated Tumescence</em></p><p><em>-NO Production by Activation of Nitric Oxide Synthase Isoforms</em></p><p><em>-Disruptions of NO-cGMP Pathway and Compensatory Mechanisms</em></p><p><em></em></p><p><em>-Additional Pro-Erectile Signalling Pathways</em></p><p><em>-cAMP/PKA Pathway</em></p><p><em>-Vasoactive Intestinal Peptide</em></p><p><em>-Prostanoids (Involved in Tumescence and Detumescence)</em></p><p><em>-Acetylcholine</em></p><p><em>-Noradrenaline-Mediated Detumescence</em></p><p><em></em></p><p><em>-Other Signalling Pathways Involved in Detumescence </em></p><p><em>-Endothelin-1</em></p><p><em>-Angiotensin II</em></p><p><em></em></p><p><em></em></p><p><em><strong>*Link between Endocrine Disrupting Chemicals and Erectile Dysfunction </strong></em></p><p><em>-Effects of Estrogenic-EDCs and Endogenous Estrogen Signalling on Erectile Function</em></p><p><em>-Indirect and Direct Mechanisms for ED Induced by Estrogenic-EDCs</em></p><p><em>-Potential Role of EDCs in Human ED and Other Aspects of Male Reproductive Health</em></p><p></p><p></p><p></p><p></p><p><strong>Conclusion</strong></p><p></p><p><em><strong>ED is extremely prevalent globally and presents major lifestyle and health problems for affected individuals and their partners. The rapid increase in prevalence cannot be accounted for by genetics and age alone; environmental factors must also play a role. Thus, it is critical to understand this condition and the underlying biology of erectile function. <u>This review summarised the complex interplay between neural, vascular, molecular, and hormonal mechanisms which govern erectile function; disruptions to any of these factors are considered risk factors for ED</u>. <u>However, the role of EDCs as risk factors for ED is starkly under-researched</u>. <u>This is despite established knowledge that androgens and potentially endogenous estrogens are both critical for erectile function in both developmental and adult physiological contexts, EDCs are pervasive in our environment, and multiple animal studies strongly suggest EDCs are among the risk factors for human ED</u>. Thus, this area needs far greater attention in order to reduce ED prevalence and avert the plethora of health hazards presented by EDCs.</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 211201, member: 13851"] [B]Abstract[/B] [I]Erectile dysfunction (ED) is one of the most prevalent chronic conditions affecting men. [B]ED can arise from disruptions during development, affecting the patterning of erectile tissues in the penis and/or disruptions in adulthood that impact sexual stimuli, neural pathways, molecular changes, and endocrine signalling that are required to drive erection.[/B] Sexual stimulation activates the parasympathetic system which causes nerve terminals in the penis to release nitric oxide (NO). As a result, the penile blood vessels dilate, allowing the penis to engorge with blood. This expansion subsequently compresses the veins surrounding the erectile tissue, restricting venous outflow. As a result, the blood pressure localised in the penis increases dramatically to produce a rigid erection, a process known as tumescence. The sympathetic pathway releases noradrenaline (NA) which causes detumescence: the reversion of the penis to the flaccid state. [B]Androgen signalling is critical for erectile function through its role in penis development and in regulating the physiological processes driving erection in the adult. Interestingly, estrogen signaling is also implicated in penis development and potentially in processes that regulate erectile function during adulthood. Given that endocrine signalling has a prominent role in erectile function, it is likely that exposure to endocrine-disrupting chemicals (EDCs) is a risk factor for ED, although this is an under-researched field.[/B] Thus, our review provides a detailed description of the underlying biology of erectile function with a focus on the role of endocrine signalling, exploring the potential link between EDCs and ED based on animal and human studies.[/I] [B]Erectile Dysfunction[/B] [I]Erectile Dysfunction Erectile Dysfunction (ED) is defined as the consistent or repeated inability to acquire or sustain an erection sufficient for satisfactory sexual performance [McCabe et al., 2016]. The 5-item International Index of Erectile Function (IIEF-5) self-questionnaire categorizes the severity of ED based on the numerical score (each of the 5 questions is worth 5 points) as no ED (22–25), mild (17–21), mild to moderate (12–16), moderate (8–11), or severe (1–7) [Rhoden et al., 2002]. [B]The erectile function relies on a combination of organic (structural, neurologic, vascular, and endocrine) and psychogenic factors. Thus, ED can have a number of aetiologies that are broadly classified as either organic or psychogenic [Johannes et al., 2000]. [U]Psychogenic risk factors[/U] for ED include depression and anxiety [Yang et al., 2019], although these are beyond the scope of this review. [U]Organic risk factors[/U] include vascular, neurologic, and endocrine abnormalities [reviewed in Ludwig and Phillips, 2014].[/B] Interestingly, since the penile vascular tissue that is responsible for an erection is a component of the global vascular system, ED of vascular origin is often an indicator of systemic endothelial dysfunction [Virag et al., 1981]. Thus, ED not only disrupts the quality of life but can also be a strong indicator of cardiovascular disease [Gandaglia et al., 2014].[/I] [B]Physiology of Erectile Function [/B] [I]-Neural Stimulation -Anatomy, Vasculature, and Hemodynamics of Erection -Calcium-Mediated Penile Smooth Muscle Contraction/Relaxation and RhoA/Rho KinaseMediated Calcium Sensitisation -Nitric Oxide (NO)-cGMP Mediated Tumescence -NO Production by Activation of Nitric Oxide Synthase Isoforms -Disruptions of NO-cGMP Pathway and Compensatory Mechanisms -Additional Pro-Erectile Signalling Pathways -cAMP/PKA Pathway -Vasoactive Intestinal Peptide -Prostanoids (Involved in Tumescence and Detumescence) -Acetylcholine -Noradrenaline-Mediated Detumescence -Other Signalling Pathways Involved in Detumescence -Endothelin-1 -Angiotensin II [B]*Link between Endocrine Disrupting Chemicals and Erectile Dysfunction [/B] -Effects of Estrogenic-EDCs and Endogenous Estrogen Signalling on Erectile Function -Indirect and Direct Mechanisms for ED Induced by Estrogenic-EDCs -Potential Role of EDCs in Human ED and Other Aspects of Male Reproductive Health[/I] [B]Conclusion[/B] [I][B]ED is extremely prevalent globally and presents major lifestyle and health problems for affected individuals and their partners. The rapid increase in prevalence cannot be accounted for by genetics and age alone; environmental factors must also play a role. Thus, it is critical to understand this condition and the underlying biology of erectile function. [U]This review summarised the complex interplay between neural, vascular, molecular, and hormonal mechanisms which govern erectile function; disruptions to any of these factors are considered risk factors for ED[/U]. [U]However, the role of EDCs as risk factors for ED is starkly under-researched[/U]. [U]This is despite established knowledge that androgens and potentially endogenous estrogens are both critical for erectile function in both developmental and adult physiological contexts, EDCs are pervasive in our environment, and multiple animal studies strongly suggest EDCs are among the risk factors for human ED[/U]. Thus, this area needs far greater attention in order to reduce ED prevalence and avert the plethora of health hazards presented by EDCs.[/B][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
When Testosterone Is Not Enough
ED in Men on the Rise: Is There a Link with Endocrine Disrupting Chemicals?
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