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Diagnosis and Management of Obstructive Sleep Apnea
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<blockquote data-quote="madman" data-source="post: 235258" data-attributes="member: 13851"><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/obstructive-sleep-apnea-and-testosterone-deficiency.18559/[/URL]</p><p></p><p><em><strong>*TRT aggravates OSA through several physiologic mechanisms including <u>neuromuscular changes to the airways, changes in metabolic requirements, and</u></strong></em><strong><em><u> changes in the physiologic response to hypoxia and hypercapnia</u></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/obstructive-sleep-apnea-and-testosterone-therapy.21325/[/URL]</p><p></p><p><strong><em><strong>CONCLUSION</strong></em></strong></p><p><strong><em><strong></strong></em></strong></p><p><strong><em><strong>As TTh is increasingly used, it is important to understand its potential adverse effects. The idea that TTh may exacerbate OSA dates back more than 40 years. For several decades, the association was explored using only case studies or small uncontrolled case series, which suggested that TTh worsened OSA. As larger cohort studies and RCTs became available, this relationship has been questioned. <u>The best current evidence suggests that short-term, high-dose testosterone administration mildly worsens OSA</u>. Longer-term TTh in subjects undergoing concomitant weight loss was shown to mildly worsen OSA but only initially. By 18 weeks, patients demonstrated a return to baseline levels of OSA risk.</strong> <strong>These results suggest that TTh's role in exacerbating OSA is small and may be time-limited. However, it is also possible that weight loss acted as a confounding factor. Additional studies are needed to determine if men who are more obese at baseline have a higher risk of developing OSA with TTh than nonobese men.</strong> <strong><em>Why testosterone would have a time-dependent effect, however, remains unanswered. <u>Regarding the mechanisms by which TTh may worsen OSA, anatomic TTh-induced airway changes and altered sleep stage architecture have been largely refuted</u>. <u>The mechanism of action is more likely related to altered hypoxic and hypercapnic ventilatory response with testosterone administration, though work is still needed to resolve inconsistencies in currently available studies</u>. Until these questions are more fully understood, clinicians may choose to exercise caution in prescribing TTh to individuals with severe, untreated OSA.</em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/obstructive-sleep-apnea-and-trt.21725/[/URL]</p><p></p><p><strong><em><strong><em><strong>Conclusion </strong></em></strong></em></strong></p><p><strong><em><strong><em></em></strong></em></strong></p><p><strong><em><strong><em><em><strong>In summary, this review summarizes the evidence on the mechanisms involved in the pathogenesis of hypogonadism in patients with OSAS, such as the abnormal circadian rhythm of gonadotrophin secretory patterns associated with obesity. TRT may represent a risk factor for OSA development and therefore, respiratory function monitoring is recommended especially in obese patients during TRT. Scanty evidence has been released on the effect of TRT in patients with OSA. <u>Data from recent randomized placebo-controlled studies address TRT as a time-dependent influence on nocturnal hypoxia, showing a positive impact after a long time of exposure</u>. Also, CPAP and PDE5i can be considered safe procedures to ameliorate sexuality in hypogonadal patients with OSA. We suggest using TRT cautiously in obese hypogonadal patients with hypoventilatory syndrome especially if they are not on CPAP. The latter aspect needs to be further confirmed by larger controlled studies.</strong></em></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/cpap-therapy-in-osa-patients-with-ed.21848/[/URL]</p><p></p><p><strong><em><strong><em><strong>Conclusion</strong></em></strong></em></strong></p><p><strong><em><strong><em></em></strong></em></strong></p><p><strong><em><strong><em><em><strong>Previously, a number of researchers paid attention to studying the relationship between OSA and ED while a small number of participants from each study were not able to draw a conclusive conclusion.<u> Utilizing the IIEF-5 scoring system in this meta-analysis found that CPAP therapy is effective in relieving the ED symptoms for male OSA patients with ED in a 3-month length setting</u>. Long-term CPAP therapy may be needed for further evaluation.</strong></em></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/can-cpap-improve-luts-and-ed-in-male-patients-with-severe-osas.21868/[/URL]</p><p></p><p><strong><em><strong><em><em><strong><strong>CONCLUSIONS</strong></strong></em></em></strong></em></strong></p><p><strong><em><strong><em><em><strong></strong></em></em></strong></em></strong></p><p><strong><em><strong><em><em><strong><em><strong><u>The results of the current study indicate that CPAP therapy provides benefits to patients with severe OSAS in terms of improvement of LUTS, nocturia, and ED</u>.</strong></em> <strong><em>Therefore, patients presenting to the urology clinic with complaints of LUTS and ED should be questioned about OSAS. Moreover, those presenting to a neurology clinic with complaints of OSAS should be asked about LUTS and ED.</em></strong> <strong><em>Better-designed studies with a larger sample size are needed to verify and support our findings.</em></strong></strong></em></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/controversies-in-testosterone-replacement-therapy-trt.22466/[/URL]</p><p></p><p><strong>Obstructive Sleep Apnea </strong></p><p></p><p><em><em><em>Liu et al26 analyzed the effect of TTh on sleep and breathing in a small double-blind, placebo-controlled, RCT, in which 17 men older than 60 years received either 3 intramuscular (IM) T injections (500 mg, 250 mg, and 250 mg) or placebo followed by the T regimen after 8 weeks of washout. The authors reported that T treatment reduced total time slept by ~1 h/night, increased the duration of hypoxemia by ~5 min/night, and disrupted breathing during sleep (total and nonrapid eye movement respiratory disturbance indices both increased by ~7 events per hour) (all P < .05). <strong>The authors concluded that short-term administration of high-dose T shortens sleep and worsens OSA in older men, but does not alter physical, mental, or metabolic function. These changes did not appear to be due to upper airway narrowing</strong></em></em></em></p><p><em><em><em></em></em></em></p><p><em><em><em>Killick et al27 also analyzed the association between T and breathing quality during sleep in a randomized, double-blind, placebo-controlled, parallel-group trial in which 21 obese men received either 3 IM 1000-mg T undecanoate injections or a placebo. Awake chemoreflex testing was performed at baseline, during week 6, and after the completion of week 18. The authors reported that TTh worsened sleep-disordered breathing at 6- 7 weeks, but not at 18 weeks, citing changes in ventilatory chemoreflex as a potential cause. <strong>The data from these studies26,27 provide supporting evidence that there is a positive association between TTh and the development of OSA.</strong></em></em></em></p><p><em><em><em></em></em></em></p><p><em><em><em>Cignarelli et al28 conducted a meta-analysis of 12 studies which included 388 men who were either eugonadal or hypogonadal and had OSA to assess the effect of continuous positive airway pressure (CPAP) utilization on T levels in this cohort. The authors reported that CPAP use was not associated with a change in serum total T levels (mean difference ¼ 1.08 nmol/L; 95% CI, -0.48 to 2.64; P ¼ .18). Despite the observation that serum T levels appeared to increase more in hypogonadal than in eugonadal men, these increases also failed to reach statistical significance. <strong>Thus, while TTh may be associated with an increased risk of OSA, treatment of OSA via CPAP does not appear to be associated with subsequent increases in serum T levels</strong></em></em></em></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/sleep-apnea-affects-sexual-function.22760/[/URL]</p><p></p><p><strong><em><strong><em><em><strong><em><strong>In conclusion, we found that all domains of sexual function as assessed by IIEF-5 have been affected in patients with OSA more than normal controls and IIEF-5 score is inversely related to the severity of OSA; as measured by AHI, which in turn has a complex interaction with other factors like hormones, obesity, age, and psychological status. <u>So in OSA patients, sexual dysfunction should be considered and assessed by IIEF-5 along with these factors</u>.</strong></em></strong></em></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/low-testosterone-in-men-recommendations-on-the-diagnosis-treatment-and-monitoring.23933/[/URL]</p><p></p><p><strong><em><strong>*Some authors recommend that TTh be discontinued if hematocrit is >54%, which may be reasonable while baseline hematocrit level >50% is a relative contraindication for starting testosterone therapy. <u>However, these recommendations are based on assumptions – the clinical significance of a hematocrit >54% is unknown</u></strong></em></strong></p><p><strong><em><strong></strong></em></strong></p><p><strong><em><strong>*<em><strong>The lack of increase in cardiovascular events with elevated hematocrit may be due to the fact that T acts as a <u>vasodilator and has anti-atherosclerotic effects</u> [223]. In addition, testosterone is able to decrease plasma concentrations of <u>procoagulatory substances such as fibrinogen and PAI-1 as well as Factor XII</u> [224] Isolated hematocrit elevations can be the result of insufficient fluid intake on a hot day. Only repeated measures of hematocrit >54% should be followed by concomitant administration of aspirin, bleeding, therapeutic phlebotomy, and/or discontinuation of TTh until hematocrit declines below 54%. After normalization of hematocrit levels, TTh can be continued with a reduced dosage</strong></em></strong></em></strong></p><p><strong><em><strong></strong></em></strong></p><p><strong><em><strong>*Periodic hematological assessment is, however, indicated, i.e. before TTh, then 3–4 months and 12 months in the first year of treatment, and annually thereafter. Although it is not yet clear what upper limit of hematocrit level is clinically desirable, dose adjustments may be necessary to keep hematocrit below 52–54%</strong></em></strong></p><p><strong><em><strong></strong></em></strong></p><p><strong><em><strong><em><strong>*<em><strong>Men with significant erythrocytosis (hematocrit >52%), severe untreated obstructive sleep apnea, or untreated severe congestive heart failure should not be started on treatment with TTh without prior resolution of the co-morbid condition.</strong></em></strong></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/prevalence-and-severity-of-sleep-apnea-in-men-with-high-hematocrit-on-trt.25258/[/URL]</p><p></p><p><strong><em><strong><em><strong>Conclusions</strong></em></strong></em></strong></p><p><strong><em><strong><em><strong></strong></em></strong></em></strong></p><p><strong><em><strong><em><strong><em>Men on TTH who are eugonadal and experience polycythemia have high rates of OSA. 80% of the patients undergoing the sleep study had OSA. <u>These data suggest that men with polycythemia on TTH should be screened for OSA</u>.</em></strong></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/comparing-rates-of-polycythemia-in-hypogonadal-men-using-nasal-t-gel-versus-im-tc.26063/[/URL]</p><p></p><p><strong><em><strong><em><strong><em><strong>4. Discussion</strong></em></strong></em></strong></em></strong></p><p><strong><em><strong><em><strong><em><strong></strong></em></strong></em></strong></em></strong></p><p><strong><em><strong><em><strong><em><strong><em>This is the first randomized trial to conduct a head-to-head comparison of NT gel and intramuscular TC. <u>Among the short-acting testosterone modalities, NT is dosed the most frequently and has the shortest half-life</u>. <u>This theoretically has the ability to more closely mimic the physiological release of testosterone and thus lead to fewer adverse events</u> [2]. <u>It has been shown that NT preserves spermatogenesis and gonadotropins [2], and the evidence now suggests that it also appears to avoid secondary erythrocytosis</u>. This is particularly important for comorbid men on testosterone, as polycythemia while on testosterone can increase the rates of major adverse cardiovascular events [8]. Having options to treat TD is essential for both providers and patients [9– 11].</em></strong></em></strong></em></strong></em></strong></p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/sleep-testosterone-and-cortisol-balance-and-aging-men.26113/[/URL]</p><p></p><p><strong><em><strong><em><strong><em><strong><em><strong>7 Obstructive sleep apnea </strong></em></strong></em></strong></em></strong></em></strong></p><p><strong><em><strong><em><strong><em><strong><em><strong></strong></em></strong></em></strong></em></strong></em></strong></p><p><strong><em><strong><em><strong><em><strong><em><strong>7.1 OSA, obesity, and testosterone in aging men </strong></em></strong></em></strong></em></strong></em></strong></p><p></p><p><em><strong>Testosterone therapy is widely believed to induce or worsen sleep apnea, and recent European and North American societal guidelines recommend vigilance in the detection of new OSA, and/or avoiding testosterone therapy in those with severe OSA [123, 124].</strong> Surprisingly, other national guidelines from the United Kingdom make no mention of OSA at all [125]. The issue of testosterone effects on OSA should not be ignored because two randomized controlled trials show that testosterone therapy can acutely (within 2–3 weeks) induce sleep-disordered breathing [126, 127]. Whether these adverse findings would have occurred with longer-term near-physiological testosterone replacement is uncertain because one of the studies utilized testosterone doses that resulted in sustained supraphysiological testosterone levels [127], and the other likely induced intermittent supraphysiological peaks and assessed for OSA during these peaks [126].</em></p><p><em></em></p><p><em><em><em><em>Two other randomized, placebo-controlled, parallel-group studies have partly addressed this uncertainty [128, 129]. The first study administered a testosterone patch or a matching dose-titrated placebo patch for 3 years to 108 healthy men over the age of 65 years [128]. The initial dose was 6 mg/day, which was titrated every 3 months to maintain blood testosterone levels below 34.7 nmol/liter. No significant difference in sleep-disordered breathing was detected between groups after 6, 12, 24, or 36 months of therapy. However, the method of detection was relatively insensitive and may have missed the development of mild or even moderate OSA. The second study remains the only study to purposefully administer testosterone to men with known moderate-severe OSA [129]. Sixty-seven middle-aged obese men with OSA were treated with 3 doses of testosterone undecanoate 1000 mg every 6 weeks, or a matching placebo, and received recommendations for a hypocaloric diet that caused weight loss that was comparable between the two groups. Testosterone treatment significantly increased sleep-disordered breathing by a moderate amount (10 events/hour) at week 7 (one week after the second injection of testosterone undecanoate), but not at week 18. <strong>Both studies allow for the possibility that the worsening of OSA could dissipate with longer-term therapy. Another possibility is that OSA has only been induced acutely, potentially due to transient effects on ventilatory drive [130–132].</strong></em></em></em></em></p><p><em><em><em><em></em></em></em></em></p><p><em><em><em><em>Despite these adverse effects on breathing during sleep, 18 weeks of testosterone therapy in men with OSA increased muscle mass, reduced liver fat, improved insulin sensitivity, and heightened sexual desire compared with placebo therapy [87, 133]. <strong>Studies advancing our knowledge regarding the relative risks and benefits of testosterone therapy in older men have recently become available [134], but further research is needed. More studies examining the risks and benefits of testosterone therapy in men with OSA over the longer term are required. Until such data are available, expert opinion will appropriately continue to caution against the use of testosterone therapy in men with untreated severe OSA [123].</strong></em></em></em></em></p></blockquote><p></p>
[QUOTE="madman, post: 235258, member: 13851"] [URL unfurl="true"]https://www.excelmale.com/forum/threads/obstructive-sleep-apnea-and-testosterone-deficiency.18559/[/URL] [I][B]*TRT aggravates OSA through several physiologic mechanisms including [U]neuromuscular changes to the airways, changes in metabolic requirements, and[/U][/B][/I][B][I][U] changes in the physiologic response to hypoxia and hypercapnia[/U][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/obstructive-sleep-apnea-and-testosterone-therapy.21325/[/URL] [B][I][B]CONCLUSION As TTh is increasingly used, it is important to understand its potential adverse effects. The idea that TTh may exacerbate OSA dates back more than 40 years. For several decades, the association was explored using only case studies or small uncontrolled case series, which suggested that TTh worsened OSA. As larger cohort studies and RCTs became available, this relationship has been questioned. [U]The best current evidence suggests that short-term, high-dose testosterone administration mildly worsens OSA[/U]. Longer-term TTh in subjects undergoing concomitant weight loss was shown to mildly worsen OSA but only initially. By 18 weeks, patients demonstrated a return to baseline levels of OSA risk.[/B] [B]These results suggest that TTh's role in exacerbating OSA is small and may be time-limited. However, it is also possible that weight loss acted as a confounding factor. Additional studies are needed to determine if men who are more obese at baseline have a higher risk of developing OSA with TTh than nonobese men.[/B] [B][I]Why testosterone would have a time-dependent effect, however, remains unanswered. [U]Regarding the mechanisms by which TTh may worsen OSA, anatomic TTh-induced airway changes and altered sleep stage architecture have been largely refuted[/U]. [U]The mechanism of action is more likely related to altered hypoxic and hypercapnic ventilatory response with testosterone administration, though work is still needed to resolve inconsistencies in currently available studies[/U]. Until these questions are more fully understood, clinicians may choose to exercise caution in prescribing TTh to individuals with severe, untreated OSA.[/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/obstructive-sleep-apnea-and-trt.21725/[/URL] [B][I][B][I][B]Conclusion [/B] [I][B]In summary, this review summarizes the evidence on the mechanisms involved in the pathogenesis of hypogonadism in patients with OSAS, such as the abnormal circadian rhythm of gonadotrophin secretory patterns associated with obesity. TRT may represent a risk factor for OSA development and therefore, respiratory function monitoring is recommended especially in obese patients during TRT. Scanty evidence has been released on the effect of TRT in patients with OSA. [U]Data from recent randomized placebo-controlled studies address TRT as a time-dependent influence on nocturnal hypoxia, showing a positive impact after a long time of exposure[/U]. Also, CPAP and PDE5i can be considered safe procedures to ameliorate sexuality in hypogonadal patients with OSA. We suggest using TRT cautiously in obese hypogonadal patients with hypoventilatory syndrome especially if they are not on CPAP. The latter aspect needs to be further confirmed by larger controlled studies.[/B][/I][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/cpap-therapy-in-osa-patients-with-ed.21848/[/URL] [B][I][B][I][B]Conclusion[/B] [I][B]Previously, a number of researchers paid attention to studying the relationship between OSA and ED while a small number of participants from each study were not able to draw a conclusive conclusion.[U] Utilizing the IIEF-5 scoring system in this meta-analysis found that CPAP therapy is effective in relieving the ED symptoms for male OSA patients with ED in a 3-month length setting[/U]. Long-term CPAP therapy may be needed for further evaluation.[/B][/I][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/can-cpap-improve-luts-and-ed-in-male-patients-with-severe-osas.21868/[/URL] [B][I][B][I][I][B][B]CONCLUSIONS[/B] [I][B][U]The results of the current study indicate that CPAP therapy provides benefits to patients with severe OSAS in terms of improvement of LUTS, nocturia, and ED[/U].[/B][/I] [B][I]Therefore, patients presenting to the urology clinic with complaints of LUTS and ED should be questioned about OSAS. Moreover, those presenting to a neurology clinic with complaints of OSAS should be asked about LUTS and ED.[/I][/B] [B][I]Better-designed studies with a larger sample size are needed to verify and support our findings.[/I][/B][/B][/I][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/controversies-in-testosterone-replacement-therapy-trt.22466/[/URL] [B]Obstructive Sleep Apnea [/B] [I][I][I]Liu et al26 analyzed the effect of TTh on sleep and breathing in a small double-blind, placebo-controlled, RCT, in which 17 men older than 60 years received either 3 intramuscular (IM) T injections (500 mg, 250 mg, and 250 mg) or placebo followed by the T regimen after 8 weeks of washout. The authors reported that T treatment reduced total time slept by ~1 h/night, increased the duration of hypoxemia by ~5 min/night, and disrupted breathing during sleep (total and nonrapid eye movement respiratory disturbance indices both increased by ~7 events per hour) (all P < .05). [B]The authors concluded that short-term administration of high-dose T shortens sleep and worsens OSA in older men, but does not alter physical, mental, or metabolic function. These changes did not appear to be due to upper airway narrowing[/B] Killick et al27 also analyzed the association between T and breathing quality during sleep in a randomized, double-blind, placebo-controlled, parallel-group trial in which 21 obese men received either 3 IM 1000-mg T undecanoate injections or a placebo. Awake chemoreflex testing was performed at baseline, during week 6, and after the completion of week 18. The authors reported that TTh worsened sleep-disordered breathing at 6- 7 weeks, but not at 18 weeks, citing changes in ventilatory chemoreflex as a potential cause. [B]The data from these studies26,27 provide supporting evidence that there is a positive association between TTh and the development of OSA.[/B] Cignarelli et al28 conducted a meta-analysis of 12 studies which included 388 men who were either eugonadal or hypogonadal and had OSA to assess the effect of continuous positive airway pressure (CPAP) utilization on T levels in this cohort. The authors reported that CPAP use was not associated with a change in serum total T levels (mean difference ¼ 1.08 nmol/L; 95% CI, -0.48 to 2.64; P ¼ .18). Despite the observation that serum T levels appeared to increase more in hypogonadal than in eugonadal men, these increases also failed to reach statistical significance. [B]Thus, while TTh may be associated with an increased risk of OSA, treatment of OSA via CPAP does not appear to be associated with subsequent increases in serum T levels[/B][/I][/I][/I] [URL unfurl="true"]https://www.excelmale.com/forum/threads/sleep-apnea-affects-sexual-function.22760/[/URL] [B][I][B][I][I][B][I][B]In conclusion, we found that all domains of sexual function as assessed by IIEF-5 have been affected in patients with OSA more than normal controls and IIEF-5 score is inversely related to the severity of OSA; as measured by AHI, which in turn has a complex interaction with other factors like hormones, obesity, age, and psychological status. [U]So in OSA patients, sexual dysfunction should be considered and assessed by IIEF-5 along with these factors[/U].[/B][/I][/B][/I][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/low-testosterone-in-men-recommendations-on-the-diagnosis-treatment-and-monitoring.23933/[/URL] [B][I][B]*Some authors recommend that TTh be discontinued if hematocrit is >54%, which may be reasonable while baseline hematocrit level >50% is a relative contraindication for starting testosterone therapy. [U]However, these recommendations are based on assumptions – the clinical significance of a hematocrit >54% is unknown[/U] *[I][B]The lack of increase in cardiovascular events with elevated hematocrit may be due to the fact that T acts as a [U]vasodilator and has anti-atherosclerotic effects[/U] [223]. In addition, testosterone is able to decrease plasma concentrations of [U]procoagulatory substances such as fibrinogen and PAI-1 as well as Factor XII[/U] [224] Isolated hematocrit elevations can be the result of insufficient fluid intake on a hot day. Only repeated measures of hematocrit >54% should be followed by concomitant administration of aspirin, bleeding, therapeutic phlebotomy, and/or discontinuation of TTh until hematocrit declines below 54%. After normalization of hematocrit levels, TTh can be continued with a reduced dosage[/B][/I] *Periodic hematological assessment is, however, indicated, i.e. before TTh, then 3–4 months and 12 months in the first year of treatment, and annually thereafter. Although it is not yet clear what upper limit of hematocrit level is clinically desirable, dose adjustments may be necessary to keep hematocrit below 52–54% [I][B]*[I][B]Men with significant erythrocytosis (hematocrit >52%), severe untreated obstructive sleep apnea, or untreated severe congestive heart failure should not be started on treatment with TTh without prior resolution of the co-morbid condition.[/B][/I][/B][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/prevalence-and-severity-of-sleep-apnea-in-men-with-high-hematocrit-on-trt.25258/[/URL] [B][I][B][I][B]Conclusions [I]Men on TTH who are eugonadal and experience polycythemia have high rates of OSA. 80% of the patients undergoing the sleep study had OSA. [U]These data suggest that men with polycythemia on TTH should be screened for OSA[/U].[/I][/B][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/comparing-rates-of-polycythemia-in-hypogonadal-men-using-nasal-t-gel-versus-im-tc.26063/[/URL] [B][I][B][I][B][I][B]4. Discussion [I]This is the first randomized trial to conduct a head-to-head comparison of NT gel and intramuscular TC. [U]Among the short-acting testosterone modalities, NT is dosed the most frequently and has the shortest half-life[/U]. [U]This theoretically has the ability to more closely mimic the physiological release of testosterone and thus lead to fewer adverse events[/U] [2]. [U]It has been shown that NT preserves spermatogenesis and gonadotropins [2], and the evidence now suggests that it also appears to avoid secondary erythrocytosis[/U]. This is particularly important for comorbid men on testosterone, as polycythemia while on testosterone can increase the rates of major adverse cardiovascular events [8]. Having options to treat TD is essential for both providers and patients [9– 11].[/I][/B][/I][/B][/I][/B][/I][/B] [URL unfurl="true"]https://www.excelmale.com/forum/threads/sleep-testosterone-and-cortisol-balance-and-aging-men.26113/[/URL] [B][I][B][I][B][I][B][I][B]7 Obstructive sleep apnea 7.1 OSA, obesity, and testosterone in aging men [/B][/I][/B][/I][/B][/I][/B][/I][/B] [I][B]Testosterone therapy is widely believed to induce or worsen sleep apnea, and recent European and North American societal guidelines recommend vigilance in the detection of new OSA, and/or avoiding testosterone therapy in those with severe OSA [123, 124].[/B] Surprisingly, other national guidelines from the United Kingdom make no mention of OSA at all [125]. The issue of testosterone effects on OSA should not be ignored because two randomized controlled trials show that testosterone therapy can acutely (within 2–3 weeks) induce sleep-disordered breathing [126, 127]. Whether these adverse findings would have occurred with longer-term near-physiological testosterone replacement is uncertain because one of the studies utilized testosterone doses that resulted in sustained supraphysiological testosterone levels [127], and the other likely induced intermittent supraphysiological peaks and assessed for OSA during these peaks [126]. [I][I][I]Two other randomized, placebo-controlled, parallel-group studies have partly addressed this uncertainty [128, 129]. The first study administered a testosterone patch or a matching dose-titrated placebo patch for 3 years to 108 healthy men over the age of 65 years [128]. The initial dose was 6 mg/day, which was titrated every 3 months to maintain blood testosterone levels below 34.7 nmol/liter. No significant difference in sleep-disordered breathing was detected between groups after 6, 12, 24, or 36 months of therapy. However, the method of detection was relatively insensitive and may have missed the development of mild or even moderate OSA. The second study remains the only study to purposefully administer testosterone to men with known moderate-severe OSA [129]. Sixty-seven middle-aged obese men with OSA were treated with 3 doses of testosterone undecanoate 1000 mg every 6 weeks, or a matching placebo, and received recommendations for a hypocaloric diet that caused weight loss that was comparable between the two groups. Testosterone treatment significantly increased sleep-disordered breathing by a moderate amount (10 events/hour) at week 7 (one week after the second injection of testosterone undecanoate), but not at week 18. [B]Both studies allow for the possibility that the worsening of OSA could dissipate with longer-term therapy. Another possibility is that OSA has only been induced acutely, potentially due to transient effects on ventilatory drive [130–132].[/B] Despite these adverse effects on breathing during sleep, 18 weeks of testosterone therapy in men with OSA increased muscle mass, reduced liver fat, improved insulin sensitivity, and heightened sexual desire compared with placebo therapy [87, 133]. [B]Studies advancing our knowledge regarding the relative risks and benefits of testosterone therapy in older men have recently become available [134], but further research is needed. More studies examining the risks and benefits of testosterone therapy in men with OSA over the longer term are required. Until such data are available, expert opinion will appropriately continue to caution against the use of testosterone therapy in men with untreated severe OSA [123].[/B][/I][/I][/I][/I] [/QUOTE]
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Diagnosis and Management of Obstructive Sleep Apnea
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