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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Nandrolone Experiences
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<blockquote data-quote="madman" data-source="post: 262771" data-attributes="member: 13851"><p>Having healthy testosterone levels has a protective effect on the health of the prostate.</p><p></p><p>This can be achieved using therapeutic doses of T for men diagnosed with hypogonadism.</p><p></p><p>I would be far more concerned with having low testosterone levels long-term!</p><p></p><p>Pushing TRT dose well beyond therapeutic (400-600 mg/week) serves no purpose other than the sole fact of gaining muscle/strength well beyond ones natural genetic potential.</p><p></p><p></p><p></p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/trt-and-the-prostate.24948/[/URL]</p><p></p><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/impact-of-low-free-testosterone-on-prostate-cancer.26193/[/URL]</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/#post-206877[/URL]</p><p></p><p></p><p><strong><u>BPH/LUTS</u></strong></p><p><strong></strong></p><p><strong><em>*There is no evidence that TTh either increases the risk of BPH or contributes to the worsening of LUTS</em></strong></p><p></p><p><em><strong>*At present, there is no evidence that TTh either increases the risk of BPH or contributes to the worsening of LUTS</strong></em></p><p></p><p></p><p></p><p></p><p><strong><u>PCa</u></strong></p><p><strong></strong></p><p><strong><em>*There is no evidence of increased PCa risk in men on TTh</em></strong></p><p></p><p><em><strong>*Recent evidence fails to support the longstanding fear that T therapy will increase prostate cancer risk or cause rapid growth of occult cancer</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*The relationship between testosterone and prostate cancer appears to follow a saturation curve, present in many biological systems, in which growth corresponds with a concentration of a key nutrient until a concentration is reached in which an excess of the nutrient is achieved (Figure 2).</strong> <strong>Clinical data indicate the <u>saturation point for serum T is approximately 250 ng/dL (8.68 nmol/L)</u></strong></em></p><p><em><strong></strong></em></p><p><em><strong>*There is no evidence that TTh will convert sub-clinical prostatic lesions to clinically detectable PCa</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*Nonetheless, in the absence of large-scale, long-term controlled studies, it is impossible to definitively assert the safety of TTh with regard to PCa.</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*Therefore, prior to starting TTh, a patient’s risk of PCa must be assessed using, at a minimum measurement of serum prostate-specific antigen (PSA). Pretreatment assessment should include PCa risk predictors such as age, family history of PCa, and ethnicity/race. If suspicion of PCa exists, it may be reasonable to perform a prostate biopsy if warranted by clinical presentation. Testosterone therapy may be initiated in these men if a prostate biopsy is negative</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*After initiation of TTh, patients should be monitored for prostate disease with measurement of serum PSA at 3–6 months, 12 months, and at least annually thereafter. In a subject with an increased risk of PCa urologist supervision is required</strong></em></p><p><em><strong></strong></em></p><p><em><strong>*<em><strong>An initial increase of prostate-specific antigen (PSA) and prostate volume with TTh is frequently seen over the first 2–6 months because the prostate is an androgen-dependent organ. The increase in PSA will be greatest in men with marked TD and least (or absent) in men with milder degrees of TD. The PSA level at 6 months after initiation of TTh should be used as the new baseline</strong></em></strong></em></p><p><em><strong></strong></em></p><p><em><strong>*Referral to a urologist for prostate evaluation and possible biopsy during TTh should be made with the development of a new palpable prostate abnormality on DRE or with a worrisome rise in PSA.</strong> <strong>Recommendations regarding what constitutes a concerning rise in PSA include an increase of 1.0 ng/ml over baseline PSA or a PSA velocity greater than 0.35 ng/ml per year.</strong></em></p><p></p><p></p><p></p><p></p><p></p><p><strong><u>EAU Guidelines on Sexual and Reproductive health 2023</u></strong></p><p><strong></strong></p><p><strong>3.7 Safety and follow-up in hypogonadism management </strong></p><p><strong></strong></p><p><strong></strong></p><p><strong>3.7.3 Lower urinary tract symptoms/benign prostatic hyperplasia </strong></p><p></p><p><em>Based on the assumption that prostate growth is dependent on the presence of androgens, historically testosterone therapy has raised some concerns regarding the possibility of aggravating LUTS in patients affected by benign prostatic hyperplasia (BPH) associated with prostate enlargement [100, 144].<strong> However, pre-clinical and clinical data have indicated that low rather than high androgen levels may decrease bladder capacity, alter tissue histology and decrease the ratio of smooth muscle to connective tissue, thus impairing urinary dynamics [100, 144].</strong></em></p><p><em></em></p><p><em>A trial of 60 patients undergoing testosterone therapy for six months showed no significant differences in post-void residual urine and prostate volume, while storage symptoms as measured by IPSS significantly improved, despite an increase in prostate-specific antigen (PSA) level [145]. A larger pre-treatment prostate volume was a predictive factor of improvement in LUTS. Similarly, a placebo controlled RCT including 120 hypogonadal (total testosterone < 12 nmol/L) men with MetS waitlisted for BPH surgery, showed that testosterone therapy did not result in a difference in in LUTS severity compared to placebo. Conversely, an improvement in ultrasound markers of inflammation in the expression of several pro-inflammatory genes was found in the treatment active arm [146]. A long-term study of 428 men undergoing testosterone therapy for 8 years demonstrated significant improvements in IPSS, no changes max flow rate (Qmax) and residual urine volume, but also a significant increase in prostate volume [147]. Similar data from the Registry of Hypogonadism in Men (RHYME), including 999 patients with a follow-up of 3 years, did not document any significant difference in PSA levels or total IPSS in men undergoing testosterone therapy, compared to untreated patients [148]. Similar results were reported in an Italian registry (SIAMO-NOI), collecting data from 432 hypogonadal men from 15 centres [149]. Meta-analyses have not found significant changes in LUTS between patients treated with testosterone or placebo [150-156]. </em><strong><em>According to the most recent literature, there are no grounds to discourage testosterone therapy in hypogonadal patients with BPH/LUTS and there is evidence of limited benefit from androgen administration. The only concern is related to patients with severe LUTS (IPSS > 19), as they are usually excluded from RCTs, therefore limiting the long-term safety data of testosterone therapy in this specific setting [100].</em></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong>3.7.4 Prostate cancer (PCa)</strong></p><p></p><p><em>A considerable number of observational studies have failed to demonstrate any association between circulating higher testosterone levels and PCa [157].</em><strong> <em>In contrast, studies investigating the relationship between low levels of testosterone and risk of PCa have found that men with very low levels of fT have a reduced risk of developing low-to-intermediate-grade PCa, but have a non-significantly increased chance of developing highgrade PCa [157].</em></strong><em> This peculiar pattern was also reported in trials such as the Health Professionals Follow-up Study, the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE), with varying magnitudes of significance [158].</em></p><p><em></em></p><p><em><strong>The most recent meta-analysis, including 27 placebo-controlled, RCTs, found no evidence of increased PSA levels following testosterone therapy for one year.</strong> When considering 11 studies reporting on the occurrence of PCa, the meta-analysis found no evidence of increased risk of PCa. However, a 1-year follow-up may be considered too short to draw firm conclusions on the risks of developing PCa. Furthermore, the analysis was restricted to studies with > 1-year follow-up, but no significant changes in PSA levels nor increased risk of PCa were found [151]. <strong>After 5-years’ median follow-up in three independent registry studies with > 1,000 patients undergoing testosterone therapy, PCa occurrence remained at all times below the reported incidence rate in the general population [159].</strong> <strong>Similar results were reported by a more recent large observational study including 10,311 men treated with testosterone therapy and 28,029 controls with a median follow-up of 5.3 years [160]. The same study, also showed that the risk of PCa was decreased for men in the highest tertile of testosterone therapy cumulative dose exposure as compared with controls [160]</strong></em></p><p><em><strong></strong></em></p><p><em><strong>With regards to PCa survivors, safety in terms of the risk of recurrence and progression has not yet been established. Limited data are available in the literature, with most case series not providing sufficient data to draw definitive conclusions (e.g., insufficient follow-up, small samples, lack of control arms, heterogeneity in study population and treatment regimen, etc.) [161].</strong> More recently, a meta-analysis derived from 13 studies including 608 patients, of whom 109 had a history of high-risk PCa, with follow-up of 1-189.3 months [162], suggested that testosterone therapy did not increase the risk of biochemical recurrence, <strong>but the available evidence is poor, limiting data interpretation [162].</strong> Similar considerations can be derived from another, larger meta-analysis of 21 studies [163].<strong> It is important to recognise that most of the studies analysed included lowrisk patients with Gleason score < 8 [162]. Interestingly, Valderrábano et al., recently described the design of the first RCT which assessed the safety/benefit ratio of testosterone therapy in hypogonadal men successfully treated with prostatectomy for non-aggressive prostate cancer [164]. <u>The study is still ongoing and eligible subjects are randomized to testosterone cypionate (100 mg/week) or placebo for 12 weeks, followed by another 12 weeks</u>.</strong> </em></p><p><em></em></p><p><em><strong>In conclusion, recent literature does not support an increased risk of PCa in hypogonadal men undergoing testosterone therapy.</strong> <strong><u>Although it is mandatory to avoid testosterone administration in men with advanced PCa, insufficient long-term prospective data on the safety of androgen administration in PCa survivors [163], without recurrence should prompt caution in choosing to treat symptomatic hypogonadal men in this setting</u>. <u>Specifically, patients should be fully counselled that the long-term effects of testosterone therapy in this setting are still unknown and requires further investigation</u>.</strong> <strong><u>If an occult PCa is not detected before initiation of testosterone therapy, treatment may unmask the cancer detected by an early rise in PSA over 6-9 months of therapy</u>.<u> Due to the lack of strong evidence-based data on safety, the possible use of testosterone therapy in symptomatic hypogonadal men previously treated for PCa should be fully discussed with patients and limited to low-risk individuals</u>.</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 262771, member: 13851"] Having healthy testosterone levels has a protective effect on the health of the prostate. This can be achieved using therapeutic doses of T for men diagnosed with hypogonadism. I would be far more concerned with having low testosterone levels long-term! Pushing TRT dose well beyond therapeutic (400-600 mg/week) serves no purpose other than the sole fact of gaining muscle/strength well beyond ones natural genetic potential. [URL unfurl="true"]https://www.excelmale.com/forum/threads/trt-and-the-prostate.24948/[/URL] [URL unfurl="true"]https://www.excelmale.com/forum/threads/impact-of-low-free-testosterone-on-prostate-cancer.26193/[/URL] [URL unfurl="true"]https://www.excelmale.com/forum/threads/low-testosterone-in-men-recommendations-on-the-diagnosis-treatment-and-monitoring.23933/#post-206877[/URL] [B][U]BPH/LUTS[/U] [I]*There is no evidence that TTh either increases the risk of BPH or contributes to the worsening of LUTS[/I][/B] [I][B]*At present, there is no evidence that TTh either increases the risk of BPH or contributes to the worsening of LUTS[/B][/I] [B][U]PCa[/U] [I]*There is no evidence of increased PCa risk in men on TTh[/I][/B] [I][B]*Recent evidence fails to support the longstanding fear that T therapy will increase prostate cancer risk or cause rapid growth of occult cancer *The relationship between testosterone and prostate cancer appears to follow a saturation curve, present in many biological systems, in which growth corresponds with a concentration of a key nutrient until a concentration is reached in which an excess of the nutrient is achieved (Figure 2).[/B] [B]Clinical data indicate the [U]saturation point for serum T is approximately 250 ng/dL (8.68 nmol/L)[/U] *There is no evidence that TTh will convert sub-clinical prostatic lesions to clinically detectable PCa *Nonetheless, in the absence of large-scale, long-term controlled studies, it is impossible to definitively assert the safety of TTh with regard to PCa. *Therefore, prior to starting TTh, a patient’s risk of PCa must be assessed using, at a minimum measurement of serum prostate-specific antigen (PSA). Pretreatment assessment should include PCa risk predictors such as age, family history of PCa, and ethnicity/race. If suspicion of PCa exists, it may be reasonable to perform a prostate biopsy if warranted by clinical presentation. Testosterone therapy may be initiated in these men if a prostate biopsy is negative *After initiation of TTh, patients should be monitored for prostate disease with measurement of serum PSA at 3–6 months, 12 months, and at least annually thereafter. In a subject with an increased risk of PCa urologist supervision is required *[I][B]An initial increase of prostate-specific antigen (PSA) and prostate volume with TTh is frequently seen over the first 2–6 months because the prostate is an androgen-dependent organ. The increase in PSA will be greatest in men with marked TD and least (or absent) in men with milder degrees of TD. The PSA level at 6 months after initiation of TTh should be used as the new baseline[/B][/I] *Referral to a urologist for prostate evaluation and possible biopsy during TTh should be made with the development of a new palpable prostate abnormality on DRE or with a worrisome rise in PSA.[/B] [B]Recommendations regarding what constitutes a concerning rise in PSA include an increase of 1.0 ng/ml over baseline PSA or a PSA velocity greater than 0.35 ng/ml per year.[/B][/I] [B][U]EAU Guidelines on Sexual and Reproductive health 2023[/U] 3.7 Safety and follow-up in hypogonadism management 3.7.3 Lower urinary tract symptoms/benign prostatic hyperplasia [/B] [I]Based on the assumption that prostate growth is dependent on the presence of androgens, historically testosterone therapy has raised some concerns regarding the possibility of aggravating LUTS in patients affected by benign prostatic hyperplasia (BPH) associated with prostate enlargement [100, 144].[B] However, pre-clinical and clinical data have indicated that low rather than high androgen levels may decrease bladder capacity, alter tissue histology and decrease the ratio of smooth muscle to connective tissue, thus impairing urinary dynamics [100, 144].[/B] A trial of 60 patients undergoing testosterone therapy for six months showed no significant differences in post-void residual urine and prostate volume, while storage symptoms as measured by IPSS significantly improved, despite an increase in prostate-specific antigen (PSA) level [145]. A larger pre-treatment prostate volume was a predictive factor of improvement in LUTS. Similarly, a placebo controlled RCT including 120 hypogonadal (total testosterone < 12 nmol/L) men with MetS waitlisted for BPH surgery, showed that testosterone therapy did not result in a difference in in LUTS severity compared to placebo. Conversely, an improvement in ultrasound markers of inflammation in the expression of several pro-inflammatory genes was found in the treatment active arm [146]. A long-term study of 428 men undergoing testosterone therapy for 8 years demonstrated significant improvements in IPSS, no changes max flow rate (Qmax) and residual urine volume, but also a significant increase in prostate volume [147]. Similar data from the Registry of Hypogonadism in Men (RHYME), including 999 patients with a follow-up of 3 years, did not document any significant difference in PSA levels or total IPSS in men undergoing testosterone therapy, compared to untreated patients [148]. Similar results were reported in an Italian registry (SIAMO-NOI), collecting data from 432 hypogonadal men from 15 centres [149]. Meta-analyses have not found significant changes in LUTS between patients treated with testosterone or placebo [150-156]. [/I][B][I]According to the most recent literature, there are no grounds to discourage testosterone therapy in hypogonadal patients with BPH/LUTS and there is evidence of limited benefit from androgen administration. The only concern is related to patients with severe LUTS (IPSS > 19), as they are usually excluded from RCTs, therefore limiting the long-term safety data of testosterone therapy in this specific setting [100].[/I] 3.7.4 Prostate cancer (PCa)[/B] [I]A considerable number of observational studies have failed to demonstrate any association between circulating higher testosterone levels and PCa [157].[/I][B] [I]In contrast, studies investigating the relationship between low levels of testosterone and risk of PCa have found that men with very low levels of fT have a reduced risk of developing low-to-intermediate-grade PCa, but have a non-significantly increased chance of developing highgrade PCa [157].[/I][/B][I] This peculiar pattern was also reported in trials such as the Health Professionals Follow-up Study, the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE), with varying magnitudes of significance [158]. [B]The most recent meta-analysis, including 27 placebo-controlled, RCTs, found no evidence of increased PSA levels following testosterone therapy for one year.[/B] When considering 11 studies reporting on the occurrence of PCa, the meta-analysis found no evidence of increased risk of PCa. However, a 1-year follow-up may be considered too short to draw firm conclusions on the risks of developing PCa. Furthermore, the analysis was restricted to studies with > 1-year follow-up, but no significant changes in PSA levels nor increased risk of PCa were found [151]. [B]After 5-years’ median follow-up in three independent registry studies with > 1,000 patients undergoing testosterone therapy, PCa occurrence remained at all times below the reported incidence rate in the general population [159].[/B] [B]Similar results were reported by a more recent large observational study including 10,311 men treated with testosterone therapy and 28,029 controls with a median follow-up of 5.3 years [160]. The same study, also showed that the risk of PCa was decreased for men in the highest tertile of testosterone therapy cumulative dose exposure as compared with controls [160] With regards to PCa survivors, safety in terms of the risk of recurrence and progression has not yet been established. Limited data are available in the literature, with most case series not providing sufficient data to draw definitive conclusions (e.g., insufficient follow-up, small samples, lack of control arms, heterogeneity in study population and treatment regimen, etc.) [161].[/B] More recently, a meta-analysis derived from 13 studies including 608 patients, of whom 109 had a history of high-risk PCa, with follow-up of 1-189.3 months [162], suggested that testosterone therapy did not increase the risk of biochemical recurrence, [B]but the available evidence is poor, limiting data interpretation [162].[/B] Similar considerations can be derived from another, larger meta-analysis of 21 studies [163].[B] It is important to recognise that most of the studies analysed included lowrisk patients with Gleason score < 8 [162]. Interestingly, Valderrábano et al., recently described the design of the first RCT which assessed the safety/benefit ratio of testosterone therapy in hypogonadal men successfully treated with prostatectomy for non-aggressive prostate cancer [164]. [U]The study is still ongoing and eligible subjects are randomized to testosterone cypionate (100 mg/week) or placebo for 12 weeks, followed by another 12 weeks[/U].[/B] [B]In conclusion, recent literature does not support an increased risk of PCa in hypogonadal men undergoing testosterone therapy.[/B] [B][U]Although it is mandatory to avoid testosterone administration in men with advanced PCa, insufficient long-term prospective data on the safety of androgen administration in PCa survivors [163], without recurrence should prompt caution in choosing to treat symptomatic hypogonadal men in this setting[/U]. [U]Specifically, patients should be fully counselled that the long-term effects of testosterone therapy in this setting are still unknown and requires further investigation[/U].[/B] [B][U]If an occult PCa is not detected before initiation of testosterone therapy, treatment may unmask the cancer detected by an early rise in PSA over 6-9 months of therapy[/U].[U] Due to the lack of strong evidence-based data on safety, the possible use of testosterone therapy in symptomatic hypogonadal men previously treated for PCa should be fully discussed with patients and limited to low-risk individuals[/U].[/B][/I] [/QUOTE]
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Clinical Use of Anabolics and Hormones
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Nandrolone Experiences
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