Testosterone + Men's Sexual Health

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madman

Super Moderator


Dr. Dubin is a fellowship-trained urologist and andrologist focusing on men’s health. He cares for men with fertility problems, sexual issues (erectile dysfunction, premature ejaculation, delayed ejaculation, etc.), Peyronie’s disease, low testosterone, testicular pain and other problems involving men’s genitalia. He wants to help men understand that the issues they face are normal and help them find solutions that fit their lifestyle and life goals.

In addition to providing individualized patient care, he is also passionate about providing helpful information to the community. He co-hosts a podcast, “Man Up — A Doctor’s Guide to Men’s Health,” in which he discuss various men’s health topics.




  • Why don’t men go to the doctor?
  • Where do men get most of their sex ed from?
  • Figuring out the difference between erections, orgasm, ejaculation (and refractory time) and desire.
  • The five things you need to get a good erection.
  • The role of testosterone and libido and erections.
  • Taking testosterone can cause infertility in 60% of men.
  • Once you take Testosterone are you going to be on it forever?
  • When a man goes to the doctor for Viagra, should the doctor ask about the partner?
  • We need more people talking about intimacy without an erect penis.
  • And if you are comfortable – what to do when you penis doesn’t work – I hear over and over about men being able to orgasm with a soft penis and I need some info on this! Are you the person? So many people think sex is over when the penis doesn’t work and I need someone to tackle this difficult topic.
  • Dr. Dubin did a study looking at women getting blamed for their partner’s erectile dysfunction. 1 out of 7 women were blamed.
  • Tips for when your male partner doesn’t want to talk about intimate issues.
  • What is with products that make you make more semen?
  • What is with penis enlarging procedures?
  • Social media inaccuracies with men’s health – sperm retention!
  • Does ejaculating decrease prostate cancer?
  • Does vasectomy cause prostate cancer?



Chapters:

00:00 Introduction and Focus on Men's Sexual Health
02:10 Stigma and Hesitancy in Seeking Help
09:55 Understanding Sexual Function: Libido, Erections, Orgasm, and Ejaculation
16:47 Testosterone and Treatment Options
21:26 Considering Overall Well-being and Quality of Life
27:00 The Role of Communication and Education in Sexual Health
32:39 Expanding the Definition of Sex and Pleasure
34:07 Resources for Further Education and Support
34:54 Understanding and Addressing Erectile Dysfunction
55:52 Debunking Myths about Semen Retention and Penis Enlargement
59:47 The Importance of Communication in Sexual Health
01:03:02 The Relationship Between Ejaculation and Prostate Cancer
01:05:07 The Safety and Benefits of Vasectomy
 
Defy Medical TRT clinic doctor
14:20-16:47 (erections/erectile dysfunction)


You need 5 things to get a good erection:


1. good blood flow
2. good nerves
3. good testosterone levels
4. neurotransmitters/arousal
5. state of mind
 
Much more to the story when it comes to testosterones impact on libido/erectile function!


*Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

*Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!


*Have realistic expectations especially when it comes to libido and erectile function!



LIBIDO


*The male sexual response cycle is complex and the exact role of testosterone in mediating libido, arousal, erection, ejaculation, and orgasm is multifactorial

*This hormone isn’t the only biological factor with clear, substantial power over our libidos





Libido starts in the brain.

Neurotransmitters have a big impact especially dopamine.

There is a fine balance here when it comes to the dopamine system!

This is key here..... dopamine circuits are powerfully regulated by androgens!


*dopamine circuits are powerfully regulated by androgens

*androgens as potent modulators of prefrontal cortical operations and of closely related, functionally critical measures of prefrontal dopamine level or tone

*androgens dynamically control meso prefrontal dopamine systems and impact prefrontal states of hypo- and hyper-dopaminergia

*dopamine-dependent prefrontal operations appear to universally follow inverted U shaped functions

* androgens maintain a lifelong capacity to bidirectionally modulate prefrontal dopamine tone

*By targeting enzymes and signaling molecules associated with androgenic metabolites of testosterone (Fig 1), these studies more directly implicate androgens in modulating prefrontal function. They also show that both supranormal androgen stimulation and androgen deficiency negatively affects prefrontal operations (Fig 2A). This inverted U- shaped function is similar to that described for functional meso prefrontal dopamine settings (Cools R and D'Esposito M, 2011; Cools R et al.,2019; Floresco SB, 2013; Floresco SB and Magyar O, 2006)

*The data also demonstrate an inverted U-shaped function that describes these dopamine effects. According to this function, prefrontal dopamine levels— often referred to as prefrontal dopamine tone- that are either higher or lower than a functionally optimal set point are detrimental to behavior and circuit function (Fig 2B).






*Again having a healthy FT is only one piece of the puzzle as libido let alone ED are multifactorial.

*Getting quality sleep, minimizing stress (physical/mental), following a healthy diet, exercising/staying active, improving overall vascular health will have a far bigger impact than jacking up your trough FT!


*Have realistic expectations especially when it comes to libido and erectile function!








ERECTILE FUNCTION

*Studies have shown that once T drops below a threshold of roughly 230 ng/dL, men can begin to experience ED.





* ED only occurs with very low testosterone levels

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Testosterone Replacement Therapy

Low testosterone levels can decrease sex drive and lead to weak erections, though this is rarely the sole cause of erectile dysfunction. Over time, the hormone deficiency can cause penile tissues to atrophy, making erections even more difficult. The condition is easily treatable with testosterone replacement therapy, which can also improve the effectiveness of oral medications. But it’s important to work alongside a doctor to monitor the condition.





*Testosterone replacement therapy can improve several aspects of sexual life, including erection, only in hypogonadal subjects but its contribution alone is clinically effective only in milder forms of erectile dysfunction





CONCLUSIONS AND FUTURE RESEARCH

The literature presented herein illustrates that T mediates erectile function, but it is imperative to note that T is not necessary for satisfactory erections. Two small prospective studies found that erectile responses to visual erotic stimuli were equivalent between hypogonadal men and healthy controls [61, 62]. However, nocturnal penile tumescence and spontaneous daytime erections were diminished in hypogonadal men. This points to the observation that motivation and interest through sexual stimuli can overcome deficiencies in the physiology of the erectile response brought upon by hypogonadism.


Several questions remain despite the robust literature that exists. In the physiology realm, certain pathways may present an opportunity for novel drug targets. For example, the study that examined castration-induced upregulation of sphingosine-1- phosphate and consequent contraction of rat CCSM showed that administering an S1P receptor antagonist reinstated CCSM relaxation [33]. From the structural aspect, corporal cavernosal fibrosis is associated with T deprivation but few studies have assessed the restorative effects of T on animal models of PD.

Clinically, the optimal population of men with ED who will benefit most from TRT is unclear. There were inconsistent results on the impact of age on treatment efficacy and while multiple RCTs have focused on just older men, a parallel large study on younger men is still lacking. The threshold of ED and T deficiency severity for which TRT is efficacious, the dosing of TRT, the timing for initiating combination therapy, and the duration of the treatment have yet to be outlined in clinical guidelines. Presumably, TRT monotherapy could be first-line for patients with severe T deficiency but milder forms of ED (with PDE5i as salvage therapy if the response is poor), whereas combination TRT and PDE5i would be first-line for those with severe T deficiency and severe ED.









Conclusions

In conclusion, this review summarizes the endogenous androgen neuroendocrine system and describes studies evaluating the role of T in human sexual desire and function. Limitations of this review include study inclusion criteria, which did not analyze studies published in languages other than English. Future systematic reviews should be conducted to further analyze the current literature in a regimented manner. Sexual desire is a sequela of complex multifactorial interactions among various biopsychosocial influences.

Both animal and human studies have solidified the role of androgens in the neuroendocrine pathways that regulate sexual desire, and this association has been validated in numerous clinical studies. The strong relationship between T and sexual desire underlies the clinical foundation of TRT in hypogonadal men, with data suggesting increased efficacy in a dose-dependent manner and with the superiority of gel over patch application.






*It is important to recognize that, whatever outcome is considered, the effects of TRT are clearly evident only in the presence of hypogonadal status (ie, total T < 12 nmol/L), whereas the positive effects of TRT are no longer confirmed for higher T levels. In addition, TRT alone can be effective in restoring only milder forms of ED, whereas combined therapy with other drugs is required when more severe vascular damage is present





Conclusion


Both animal and human studies support an association between hypogonadism and ED. Animal studies first elucidated testosterone’s role in maintaining the proper synthesis and/or release of enzymes as well as tissue structure and function in the corpora cavernosa. When low testosterone is present in both animals and humans, erectile function is compromised as a result, which can be improved with testosterone replacement.

Testosterone monotherapy in hypogonadal men without significant comorbidities can improve erectile function in those struggling with ED. Combination therapy with testosterone and PDE-5 inhibitors can lead to improvement in erectile function for hypogonadal men with medical comorbidities who do not respond to monotherapy. Based on the evidence, it is important to screen all men with ED for hypogonadism, especially those with a history of inadequate response to PDE-5 inhibitors, so that the appropriate treatment plan is implemented. Further studies are crucial to better understand the nuances of testosterone treatment for patients with different degrees of hypogonadism and to optimize sexual outcomes in hypogonadal men with ED.






Erectile Dysfunction

Erectile dysfunction (ED) is defined as, “an impairment in the arousal phase of [the male] sexual response” with “consistent or recurrent inability to attain and/or maintain penile erection sufficient for sexual satisfaction, including satisfactory sexual performance.”20

The prevalence of ED has been widely reported by a variety of sources. Approximately 20 percent of adult men are reported to have ED.21

ED is typically classified as psychogenic or organic.22 The pathogenesis of ED is multifactorial and can involve multiple underlying disturbances, including vasculogenic, neurogenic, hormonal, and/or medication-induced.

Although most men with ED do not have hypogonadism, ED has been shown to be related to low T levels in some cases. It has been postulated that T may exert local effects to mediate erections based on studies demonstrating fluctuations in serum and corporal T levels during erection.23 Studies have shown that once T drops below a threshold of roughly 230 ng/dL, men can begin to experience ED.21 This is particularly relevant for men undergoing ADT, for whom ED is a well-established potential side effect. Further research is being undertaken to better understand the mechanisms by which hypogonadism affects erectile function.

Low Libido

Meta-analyses investigating the effect of TRT on male sexual function have demonstrated variable improvements in libido. In these studies, TRT led to reported improvements specifically in hypogonadal men, with no change in libido for eugonadal men.32 Furthermore, the benefits of TRT were found to be greater in men with lower baseline levels of T (< 288 ng/dL).35 Although the literature suggests that TRT can improve libido in hypogonadal men, some studies have shown no significant difference in sexual satisfaction after TRT.36




Erectile Dysfunction

In hypogonadal men, TRT has been shown to improve responses to PDE5 inhibitors (PDE5i) for ED.37 Several randomized controlled trials and systematic reviews of hypogonadal men with ED have shown that PDE5i therapy in conjunction with TRT is more effective in improving ED than PDE5i therapy or TRT alone.24,28 Therefore, the AUA recommends that urologists inform hypogonadal men with ED that PDE5i therapy may be augmented by TRT.24

While TRT in hypogonadal men may optimize the efficacy of other ED treatments by restoring normal T levels, there is not adequate data to support combining TRT with other ED treatments.

Similarly, TRT is not recommended as a monotherapy for ED.30
 
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