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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
AAS abuse produces a significant increase in aortic stiffness
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<blockquote data-quote="madman" data-source="post: 189023" data-attributes="member: 13851"><p>With trt we are replacing physiological levels of the primary sex hormone and anabolic steroid in males which is responsible for the beneficial effects (mood, energy, libido, erectile function, muscle, strength, recovery, cardiovascular, brain, bone, immune system).</p><p></p><p>Having healthy T levels would be cardiovascular protective.</p><p></p><p>My protocol was 150 mg/week (75 mg every 3.5 days).</p><p></p><p>Currently 120 mg/week (60 mg every 3.5 days).</p><p></p><p>I have always run my TT/FT levels on the higher-end physiological range.</p><p></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/loh-reductio-ad-absurdum-of-the-cardiovascular-risk%E2%80%93benefit-of-trt.21455/[/URL]</p><p></p><p></p><p><strong>Conclusion</strong></p><p></p><p><em><strong><span style="color: rgb(184, 49, 47)">Using the reductio ad absurdum logic, we contradicted the initial assumption of an overall harmful effect of T on the CV system. </span><span style="color: rgb(44, 130, 201)"><u>Although T has been demonstrated to have overall favorable effects on vasomotion, arterial stiffness, atherosclerosis, cardiac electrophysiology, oxygen delivery, cardiac contractility, and remodeling</u>,</span> </strong><span style="color: rgb(184, 49, 47)"><strong>it possesses a prothrombotic effect due to its action on platelet function and blood viscosity</strong>.</span></em> <strong><em><span style="color: rgb(44, 130, 201)"><u>In summary, based on the current evidence, CV disease does not appear to be increased in patients undergoing TRT</u>.178,179</span></em></strong> <strong><em><span style="color: rgb(184, 49, 47)">Most physicians against TRT will argue that TRT is “neutral” in terms of CV safety. While the latter is possible, the indication for TRT has never been to address CV dysfunction but rather to improve various signs and symptoms in LOH that correlate well with low testosterone levels. </span>Nonetheless, in older patients with a known CV risk factor, a tailored approach is suggested.14,25 Symptoms, comorbidities, baseline and target levels of T, formulation, and therapy timing25,180,181 should be considered to improve sexual function, mood, depressive symptoms, and the mobility of patients with low testosterone levels.13,33,182,183</em></strong></p><p></p><p></p><p></p><p></p><p></p><p></p><p>[ATTACH=full]11137[/ATTACH]</p><p>[ATTACH=full]11138[/ATTACH]</p><p>[ATTACH=full]11139[/ATTACH]</p><p><strong>Table 1. <span style="color: rgb(184, 49, 47)">Summary of the effects of testosterone on the vessel and endothelial function: small, medium, large vessels.</span> <span style="color: rgb(44, 130, 201)"><u>Coronary arteries vasomotion</u>.</span> Testosterone exerts a vasodilating action through a rapid, non-genomic, and endothelial-independent action on K and Ca channels. Moreover, it has also an endothelial-dependent vasodilating effect mediated by NO. <span style="color: rgb(44, 130, 201)"><u>Peripheral arterial stiffness.</u></span><span style="color: rgb(184, 49, 47)"><u> Testosterone reduces arterial stiffness through, an androgen receptor-dependent modulation of apoptosis and senescence of vascular smooth muscle cells</u>. Testosterone vasodilating action and anti-inflammatory effects may also have a role. </span><span style="color: rgb(44, 130, 201)"><u>Large vessel atherosclerosis</u>.</span> Testosterone exerts several anti-atherogenic actions, including an anti-inflammatory effect which may hinder the initial development of atheroma. The effect on VSMSs is complex and may be reliant on the stage of plaque development. VSMCs migration and proliferation could be considered protective against plaque destabilization, while VSMCs apoptosis could be responsible for plaque vulnerability.</strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong><strong>Figure legend: Fig. 1 <span style="color: rgb(184, 49, 47)">Summary of testosterone cardiovascular (CV) effects.</span> Created with images adapted from SMART - Servier Medical Art <span style="color: rgb(184, 49, 47)">(<a href="http://smart.servier.com/" target="_blank">SMART - Servier Medical ART</a>)</span>, licensed under a Creative Common Attribution 3.0 License <span style="color: rgb(184, 49, 47)">(<a href="https://creativecommons.org/licenses/by/3.0" target="_blank">Creative Commons — Attribution 3.0 Unported — CC BY 3.0</a>)</span></strong> </strong></p><p>[ATTACH=full]11140[/ATTACH]</p></blockquote><p></p>
[QUOTE="madman, post: 189023, member: 13851"] With trt we are replacing physiological levels of the primary sex hormone and anabolic steroid in males which is responsible for the beneficial effects (mood, energy, libido, erectile function, muscle, strength, recovery, cardiovascular, brain, bone, immune system). Having healthy T levels would be cardiovascular protective. My protocol was 150 mg/week (75 mg every 3.5 days). Currently 120 mg/week (60 mg every 3.5 days). I have always run my TT/FT levels on the higher-end physiological range. [URL unfurl="true"]https://www.excelmale.com/forum/threads/loh-reductio-ad-absurdum-of-the-cardiovascular-risk%E2%80%93benefit-of-trt.21455/[/URL] [B]Conclusion[/B] [I][B][COLOR=rgb(184, 49, 47)]Using the reductio ad absurdum logic, we contradicted the initial assumption of an overall harmful effect of T on the CV system. [/COLOR][COLOR=rgb(44, 130, 201)][U]Although T has been demonstrated to have overall favorable effects on vasomotion, arterial stiffness, atherosclerosis, cardiac electrophysiology, oxygen delivery, cardiac contractility, and remodeling[/U],[/COLOR] [/B][COLOR=rgb(184, 49, 47)][B]it possesses a prothrombotic effect due to its action on platelet function and blood viscosity[/B].[/COLOR][/I] [B][I][COLOR=rgb(44, 130, 201)][U]In summary, based on the current evidence, CV disease does not appear to be increased in patients undergoing TRT[/U].178,179[/COLOR][/I][/B] [B][I][COLOR=rgb(184, 49, 47)]Most physicians against TRT will argue that TRT is “neutral” in terms of CV safety. While the latter is possible, the indication for TRT has never been to address CV dysfunction but rather to improve various signs and symptoms in LOH that correlate well with low testosterone levels. [/COLOR]Nonetheless, in older patients with a known CV risk factor, a tailored approach is suggested.14,25 Symptoms, comorbidities, baseline and target levels of T, formulation, and therapy timing25,180,181 should be considered to improve sexual function, mood, depressive symptoms, and the mobility of patients with low testosterone levels.13,33,182,183[/I][/B] [ATTACH type="full" alt="Screenshot (2210).png"]11137[/ATTACH] [ATTACH type="full" alt="Screenshot (2211).png"]11138[/ATTACH] [ATTACH type="full" alt="Screenshot (2212).png"]11139[/ATTACH] [B]Table 1. [COLOR=rgb(184, 49, 47)]Summary of the effects of testosterone on the vessel and endothelial function: small, medium, large vessels.[/COLOR] [COLOR=rgb(44, 130, 201)][U]Coronary arteries vasomotion[/U].[/COLOR] Testosterone exerts a vasodilating action through a rapid, non-genomic, and endothelial-independent action on K and Ca channels. Moreover, it has also an endothelial-dependent vasodilating effect mediated by NO. [COLOR=rgb(44, 130, 201)][U]Peripheral arterial stiffness.[/U][/COLOR][COLOR=rgb(184, 49, 47)][U] Testosterone reduces arterial stiffness through, an androgen receptor-dependent modulation of apoptosis and senescence of vascular smooth muscle cells[/U]. Testosterone vasodilating action and anti-inflammatory effects may also have a role. [/COLOR][COLOR=rgb(44, 130, 201)][U]Large vessel atherosclerosis[/U].[/COLOR] Testosterone exerts several anti-atherogenic actions, including an anti-inflammatory effect which may hinder the initial development of atheroma. The effect on VSMSs is complex and may be reliant on the stage of plaque development. VSMCs migration and proliferation could be considered protective against plaque destabilization, while VSMCs apoptosis could be responsible for plaque vulnerability. [B]Figure legend: Fig. 1 [COLOR=rgb(184, 49, 47)]Summary of testosterone cardiovascular (CV) effects.[/COLOR] Created with images adapted from SMART - Servier Medical Art [COLOR=rgb(184, 49, 47)]([URL='http://smart.servier.com/']SMART - Servier Medical ART[/URL])[/COLOR], licensed under a Creative Common Attribution 3.0 License [COLOR=rgb(184, 49, 47)]([URL='https://creativecommons.org/licenses/by/3.0']Creative Commons — Attribution 3.0 Unported — CC BY 3.0[/URL])[/COLOR][/B] [/B] [ATTACH type="full" alt="Screenshot (2213).png"]11140[/ATTACH] [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
AAS abuse produces a significant increase in aortic stiffness
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