Penis smaller after TRT

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equel

Active Member
My advice wasn't for OP only as there seemed to be many others on TRT who noticed shrinkage.

Ageing lol? I am 30 years old and I don't have ED. Viagra still gives the wow effect and makes me pop random boners all the time while cialis does not do absolutely anything anymore as I have developed tolerance after taking it for years. There are many others with similar experience. You definitely develop a tolerance to PDE5 inhibitors.

What's with your attitude, mr know it all? Go take an AI and calm down.

Also, taking proviron is good advice. Fix the androgen to estrogen balance rather than decreasing test or taking needless aromatase inhibitors which are not good for you at all.

ye madman is some grumpy old dude, always shit attitude


anyway, this is e2 related, most likely too high e2, i get it aswell when e2 is messed up, not even viagra or cialis help (much).

When my e2 is high, I can get an erection but it goes down very quick, even with viagra, cialis, all kinds of shit.

fix e2/t ratio and ull be fine.
 
Defy Medical TRT clinic doctor

eli

Active Member
I've used Cialis/ viagra for 13 years, nothing has changed. Works everytime, no tolerance built up.

Maybe your libido took a hit or something.

The only time viagra/cialis don't work for me is when E2 is either too high or too low.

AIs are honestly shit, destroys my libido for a few weeks no matter what dose.

If you're low SHBG, I'd stay clear away from DHT derivatives such as Proviron etc, they only work great with medium to high SHBG guys.
 

Drug350

Member
I just started TRT and I've noticed my member is definitely larger, especially flaccid, now vs prior to TRT. I think mine got smaller because of my low Testosterone levels and as soon as I started, it grew right back to original size.
As far as "guys getting older and because of less blood supply, it gets smaller", I think it's because as you get older most guys tend to put on belly fat and gain a lot of fat just above the penis, a "fat pad" which ultimately makes your penis look smaller. Loose weight and your member will look larger.
 

DixieWrecked

Well-Known Member
I just started TRT and I've noticed my member is definitely larger, especially flaccid, now vs prior to TRT. I think mine got smaller because of my low Testosterone levels and as soon as I started, it grew right back to original size.
As far as "guys getting older and because of less blood supply, it gets smaller", I think it's because as you get older most guys tend to put on belly fat and gain a lot of fat just above the penis, a "fat pad" which ultimately makes your penis look smaller. Loose weight and your member will look larger.
Let us know how things are going after more time.
 

Mastodont

Active Member
This was a fascinating thread, i always had this problem, but trt seemed to worsen it, but there was always once in a while a time window, usually very soon after injection when blood flow increased and balls dropped down for a while. Must have something to do with aromatase generating estradiol with a delay. This problem is clearly made worse by any kind of stress, and for myself, any exercise has always seemed to cause shrinkage. Cold weather seems to keep the balls constantly elevated too. I dont have high estradiol at all when off trt so there must be other things going on besides estradiol being too high, overstimulation from testosterone induces anxiety which seems a very logical reason for a tight scrotum.

As an example, it always seems to be the case that i get more flaccid hang when i go on a vacation from the cold north, do not think it's just the warm weather, it is hard to say as probably anyone experiences decrease in stress level and anxiety when they are detached from their usual routines and enjoy the benefits of sunlight.
 

Simbarn

Active Member
This was a fascinating thread, i always had this problem, but trt seemed to worsen it, but there was always once in a while a time window, usually very soon after injection when blood flow increased and balls dropped down for a while. Must have something to do with aromatase generating estradiol with a delay. This problem is clearly made worse by any kind of stress, and for myself, any exercise has always seemed to cause shrinkage. Cold weather seems to keep the balls constantly elevated too. I dont have high estradiol at all when off trt so there must be other things going on besides estradiol being too high, overstimulation from testosterone induces anxiety which seems a very logical reason for a tight scrotum.

As an example, it always seems to be the case that i get more flaccid hang when i go on a vacation from the cold north, do not think it's just the warm weather, it is hard to say as probably anyone experiences decrease in stress level and anxiety when they are detached from their usual routines and enjoy the benefits of sunlight.
When you are on vacation, as you say there is less "stress", sympathetic activity is decreased in your whole nervous system. The sympathetic dominance that TRT can cause in some men is lessened in these periods of time. Adrenergic activity in the erectile tissues is reduced so smooth muscle in the penis is further relaxed and blood flow increases. The scrotum also relaxes due to the same mechanisms, not to mention the warmer weather!
 

madman

Super Moderator
My advice wasn't for OP only as there seemed to be many others on TRT who noticed shrinkage.

Ageing lol? I am 30 years old and I don't have ED. Viagra still gives the wow effect and makes me pop random boners all the time while cialis does not do absolutely anything anymore as I have developed tolerance after taking it for years. There are many others with similar experience. You definitely develop a tolerance to PDE5 inhibitors.

What's with your attitude, mr know it all? Go take an AI and calm down.

Also, taking proviron is good advice. Fix the androgen to estrogen balance rather than decreasing test or taking needless aromatase inhibitors which are not good for you at all.

Now that you have cleared that up!

Do your homework before making such statements on here son!

This is ridiculous.



post #53 (your previous reply)

It's probably mostly estrogen related. When your e2 is messed up even ed drugs do nothing.

I'd suggest trying proviron with trt and maybe doxazosin 1-2mg. I noticed benefits from HCG as well but it's not worth the e2 swings for me. With proviron and doxazosin my flaccid dick is always in "semi" state like I have just taken cialis. I used to take cialis daily but I don't recommend that to anyone anymore as you develop tolerance over years and it literally stops doing anything despite research saying otherwise. Proviron is amazing.









Look into it a Lil deeper champ!



In fact, it is safe to state that most men who respond to these PDE5 inhibitors, if they live long enough, will at some time later on in their life ultimately fail to respond to these drugs (30,31). Logic then dictates that when this lack of responsiveness occurs and barring any loss of arterial inflow, it could only be due to either (I) progression of the process within the penile tissues that are causing the ED or (II) tachyphylaxis of the PDE5 inhibitor. Since it has been demonstrated unequivocally that these PDE5 inhibitors do not undergo tachyphylaxis (32,33), one can only conclude that for those men who are suffering from ARED the subsequent diminution in their response to these PDE5 inhibitors would have to be by default the progression of the aging-related processes, in particular, the SMC apoptosis that continues to forge ahead on as one age. Once the PDE5 inhibitors become incapable at its highest dose of inducing sufficient tumescence to allow sexual activity to occur where it was previously able to do so, it merely identifies the time has been reached when either the remaining functioning corporal smooth muscle is incapable via the oral route of drug administration of achieving sufficient relaxation to allow the attainment of an intra-corporeal pressure high enough to compress the subtunical veins (increasing venous leakage) or there has been a concomitant decrease in the inflow of blood into the penis which is incapable of providing enough blood to the corporal sinusoids (arteriogenic dysfunction) to allow for any veno-occlusion to occur or it could be due to a little bit of both of these processes. Since an erection is simply a mechanical event requiring a dynamic balance between inflow and outflow of blood within the corporal sinusoids, the determination of whether one or both processes are functioning normally in an individual patient requires an individual evaluation of each of these processes (17,20).




post #5





post #6

Penile Vascular Protection

The medical literature widely supports vascular health objectives as a means toward achieving long-term health maintenance and longevity. Several thought leaders in sexual medicine have further pointed to penile vascular health as a critical gauge of this outcome (Kloner et al, 2003; Solomon et al, 2003). The pathogenesis of vascular disease both systemically and locally in the penis is linked with NO imbalance via endothelial defects and/or oxidative stress, which subsequently diminishes the physiologic actions of NO and its effectors (Cooke and Dzau, 1997; Bonetti et al, 2003) (Figure 4). To address this pathophysiology, suggested preventative practices have been advocated to include increasing physical fitness, improving healthful dietary habits, and reducing obesity (Esposito et al, 2004; Esposito et al, 2006). Additional consideration has been given to medical therapies such as regularly used PDE5 inhibitors under the premise that this treatment may afford long-term vascular healthful benefits for the penis (Montorsi et al, 2000; Burnett, 2005a).

Basic scientific evidence supports a penile vasculoprotective premise associated with long-term PDE5 inhibitor use. Several scientific studies have shown the utility of chronically applied PDE5 inhibitors in improving the structure and function of the cavernosal tissue and provided plausible mechanisms for these beneficial effects.
In experimental paradigms involving rats that were chemically diabetogenic (De Young et al, 2003; Ahn et al, 2005), intact (Behr-Roussel et al, 2005), or aged (Musicki et al, 2005b; Ferrini et al, 2007) or had cavernous nerve injuries (Vignozzi et al, 2006; Ferrini et al, 2006a; Lagoda et al, 2007), continuous systemic PDE5 inhibitor treatment ranging from several days to 3 months preserved erectile tissue morphology and erection physiology to a better extent than did control treatments. Improved erectile responses were found to be sustained after confirmed drug clearance or withdrawal of the active drug in vivo (Musicki et al, 2005a; Lagoda et al, 2007) and in vitro (Behr-Roussel et al, 2005) protocols, respectively. Foremost possible biologic mechanisms by which PDE5 inhibitors afford penile vascular protection include antioxidation (De Young et al, 2003; Lagoda et al, 2007), antiapoptosis (Ahn et al, 2005; Musicki et al, 2005b), and activation of blood flow-associated vasodilatory effectors (BehrRoussel et al, 2005; Musicki et al, 2005b; Ferrini et al, 2006a; Vignozzi et al, 2006; Ferrini et al, 2007).

A growing body of clinical literature also suggests that chronically used PDE5 inhibitors exert sustained healthful effects on the penile vasculature.
Efficacy and tolerability have been demonstrated for sildenafil and tadalafil using once-daily or alternate day dosing regimens in men with ED enrolled in uncontrolled, open-label design studies (McMahon, 2004; Caretta et al, 2005; McMahon, 2005; Mirone et al, 2005; Sommer and Schulze, 2005; Buvat et al, 2006). In clinical trials with the rigor of randomization and placebo control design, efficacy and safety endpoints have also been shown for tadalafil (Porst et al, 2006; Rajfer et al, 2007). A substantial groundswell of interest has been generated to apply this mode of therapy to the postradical prostatectomy population according to a conceptual ‘‘penile rehabilitation’’ strategy. This population experiences at least some temporary degree of ED as a consequence of the surgery, even when cavernous nerve-sparing techniques are applied (Burnett, 2005b). Much attention was paid to the placebo-controlled study involving postoperative nightly administration of sildenafil, which found a 27% return of spontaneous, normal erectile activity rate compared with the 4% rate found in the placebo arm at 1 year after surgery (Padma-Nathan et al, 2004b). In other reports involving open-label study designs, investigators attempted to define an optimal therapeutic regimen in terms of such variables as dosing schedule, duration of administration, and timing of application while also describing improvements in spontaneous erectile function resulting from chronic PDE5 inhibitor use (Gontero et al, 2005; Mulhall et al, 2005)

Several caveats should be addressed in considering the utility of long-term PDE5 inhibitor treatment for this clinical application. One early identified controversy was whether the therapeutic strategy could cause pharmacologically induced ‘‘tachyphylaxis,’’ as suggested by a report that described a 20% dose elevation rate and 17% discontinuation rate due to loss of efficacy in patients with ED using sildenafil ‘‘on-demand’’ over a 2-year interval (El-Galley et al, 2001). However, likely explanations for declines in treatment effect over the long term are underlying disease state progression, inadequate dosing, application of the therapy, relationship difficulties, and psychogenic factors (Steers, 2002). Furthermore, findings of consistent efficacy and tolerability of treatment following both long-term, ‘‘on-demand’’ schedules reported previously (Carson, 2003) and long-term, continuous dosing reported more recently (Porst et al, 2006; Rajfer et al, 2007) argue against the development of treatment tolerance. It is acknowledged that PDE5 expression levels apparently increase with continuous treatment in basic science experimental paradigms (Lin et al, 2003; Musicki et al, 2005a), but the consequence of increasing PDE5 expression above normative levels in the penis was not demonstrated to negatively impact physiologic erectile responses (Musicki et al, 2005a; Behr-Roussel et al, 2005).

Another matter for consideration is whether prophylactic PDE5 inhibitor therapy should be given only to patients with certain underlying medical conditions. Much interest exists to apply the therapy to patients with severe forms of ED or conditions that would predict the likely development of ED. In this vein, the therapy would apply to those individuals with such risk factors as diabetes, cardiovascular disease, prior pelvic surgery, and aging.
In their rat model study of chronic sildenafil dosing, Musicki et al (2005b) found that erections improved only in erection-impaired, aged rats but not in erection-intact, young rats. Compensatory homeostatic mechanisms were found to develop in young rats, suggesting to the investigators that such mechanisms are operable in the penis of the ‘‘healthy’’ individual in response to long-term PDE5 inhibitor treatment which limits supernormal erectogenic effects and concurrently prevents potentially harmful excessive erections.

Continued study is needed to confirm clinical impressions of a penile vascular protection benefit, which at this stage should be considered preliminary. Additionally, further investigation is needed to clarify molecular mechanisms associated with the presumed therapeutic benefit. Investigative work done in the cardiovascular field has shown the preconditioning effects of PDE5 inhibition against ischemic/reperfusion injury in the intact heart (Das et al, 2002; Kukreja, 2007). Cardioprotective effects have been related to activation of protein kinase C/extracellular signal-regulated kinase signaling, the opening of mitochondrial adenosine triphosphate-sensitive potassium channels, and attenuation of cell death resulting from necrosis and apoptosis (Kukreja, 2007). Further investigation may reveal whether or not such cellular or subcellular effects actually occur in the penis following long-term PDE5 inhibitor treatment. It is recognized that advancing the knowledge base in this area may occur most readily at the experimental animal model level, in which penile tissues are more easily obtained for molecular studies and objective erection testing is also more feasible. However, important inferences may still result from continued active research efforts expended at the clinical level. Recent work in men by Foresta et al (2007) showing that vardenafil increases circulating progenitor cells, which are involved in the process of neovascularization and continuous repair of the endothelium, via bone marrow stimulation has contributed to defining the endothelial protective role of PDE5 inhibitors.
 

madman

Super Moderator
ye madman is some grumpy old dude, always shit attitude


anyway, this is e2 related, most likely too high e2, i get it aswell when e2 is messed up, not even viagra or cialis help (much).

When my e2 is high, I can get an erection but it goes down very quick, even with viagra, cialis, all kinds of shit.

fix e2/t ratio and ull be fine.

Please anything but those one-liners on here!

We know why you're mad.
 

Mastodont

Active Member
I would like to try daily tadalafil to see if it improves flaccid hang but even 2.5mg raises resting heart rate and makes nosebreathing difficult.
 

equel

Active Member
Now that you have cleared that up!

Do your homework before making such statements on here son!

This is ridiculous.



post #53 (your previous reply)

It's probably mostly estrogen related. When your e2 is messed up even ed drugs do nothing.

I'd suggest trying proviron with trt and maybe doxazosin 1-2mg. I noticed benefits from HCG as well but it's not worth the e2 swings for me. With proviron and doxazosin my flaccid dick is always in "semi" state like I have just taken cialis. I used to take cialis daily but I don't recommend that to anyone anymore as you develop tolerance over years and it literally stops doing anything despite research saying otherwise. Proviron is amazing.









Look into it a Lil deeper champ!



In fact, it is safe to state that most men who respond to these PDE5 inhibitors, if they live long enough, will at some time later on in their life ultimately fail to respond to these drugs (30,31). Logic then dictates that when this lack of responsiveness occurs and barring any loss of arterial inflow, it could only be due to either (I) progression of the process within the penile tissues that are causing the ED or (II) tachyphylaxis of the PDE5 inhibitor. Since it has been demonstrated unequivocally that these PDE5 inhibitors do not undergo tachyphylaxis (32,33), one can only conclude that for those men who are suffering from ARED the subsequent diminution in their response to these PDE5 inhibitors would have to be by default the progression of the aging-related processes, in particular, the SMC apoptosis that continues to forge ahead on as one age. Once the PDE5 inhibitors become incapable at its highest dose of inducing sufficient tumescence to allow sexual activity to occur where it was previously able to do so, it merely identifies the time has been reached when either the remaining functioning corporal smooth muscle is incapable via the oral route of drug administration of achieving sufficient relaxation to allow the attainment of an intra-corporeal pressure high enough to compress the subtunical veins (increasing venous leakage) or there has been a concomitant decrease in the inflow of blood into the penis which is incapable of providing enough blood to the corporal sinusoids (arteriogenic dysfunction) to allow for any veno-occlusion to occur or it could be due to a little bit of both of these processes. Since an erection is simply a mechanical event requiring a dynamic balance between inflow and outflow of blood within the corporal sinusoids, the determination of whether one or both processes are functioning normally in an individual patient requires an individual evaluation of each of these processes (17,20).




post #5





post #6

Penile Vascular Protection

The medical literature widely supports vascular health objectives as a means toward achieving long-term health maintenance and longevity. Several thought leaders in sexual medicine have further pointed to penile vascular health as a critical gauge of this outcome (Kloner et al, 2003; Solomon et al, 2003). The pathogenesis of vascular disease both systemically and locally in the penis is linked with NO imbalance via endothelial defects and/or oxidative stress, which subsequently diminishes the physiologic actions of NO and its effectors (Cooke and Dzau, 1997; Bonetti et al, 2003) (Figure 4). To address this pathophysiology, suggested preventative practices have been advocated to include increasing physical fitness, improving healthful dietary habits, and reducing obesity (Esposito et al, 2004; Esposito et al, 2006). Additional consideration has been given to medical therapies such as regularly used PDE5 inhibitors under the premise that this treatment may afford long-term vascular healthful benefits for the penis (Montorsi et al, 2000; Burnett, 2005a).

Basic scientific evidence supports a penile vasculoprotective premise associated with long-term PDE5 inhibitor use. Several scientific studies have shown the utility of chronically applied PDE5 inhibitors in improving the structure and function of the cavernosal tissue and provided plausible mechanisms for these beneficial effects.
In experimental paradigms involving rats that were chemically diabetogenic (De Young et al, 2003; Ahn et al, 2005), intact (Behr-Roussel et al, 2005), or aged (Musicki et al, 2005b; Ferrini et al, 2007) or had cavernous nerve injuries (Vignozzi et al, 2006; Ferrini et al, 2006a; Lagoda et al, 2007), continuous systemic PDE5 inhibitor treatment ranging from several days to 3 months preserved erectile tissue morphology and erection physiology to a better extent than did control treatments. Improved erectile responses were found to be sustained after confirmed drug clearance or withdrawal of the active drug in vivo (Musicki et al, 2005a; Lagoda et al, 2007) and in vitro (Behr-Roussel et al, 2005) protocols, respectively. Foremost possible biologic mechanisms by which PDE5 inhibitors afford penile vascular protection include antioxidation (De Young et al, 2003; Lagoda et al, 2007), antiapoptosis (Ahn et al, 2005; Musicki et al, 2005b), and activation of blood flow-associated vasodilatory effectors (BehrRoussel et al, 2005; Musicki et al, 2005b; Ferrini et al, 2006a; Vignozzi et al, 2006; Ferrini et al, 2007).

A growing body of clinical literature also suggests that chronically used PDE5 inhibitors exert sustained healthful effects on the penile vasculature.
Efficacy and tolerability have been demonstrated for sildenafil and tadalafil using once-daily or alternate day dosing regimens in men with ED enrolled in uncontrolled, open-label design studies (McMahon, 2004; Caretta et al, 2005; McMahon, 2005; Mirone et al, 2005; Sommer and Schulze, 2005; Buvat et al, 2006). In clinical trials with the rigor of randomization and placebo control design, efficacy and safety endpoints have also been shown for tadalafil (Porst et al, 2006; Rajfer et al, 2007). A substantial groundswell of interest has been generated to apply this mode of therapy to the postradical prostatectomy population according to a conceptual ‘‘penile rehabilitation’’ strategy. This population experiences at least some temporary degree of ED as a consequence of the surgery, even when cavernous nerve-sparing techniques are applied (Burnett, 2005b). Much attention was paid to the placebo-controlled study involving postoperative nightly administration of sildenafil, which found a 27% return of spontaneous, normal erectile activity rate compared with the 4% rate found in the placebo arm at 1 year after surgery (Padma-Nathan et al, 2004b). In other reports involving open-label study designs, investigators attempted to define an optimal therapeutic regimen in terms of such variables as dosing schedule, duration of administration, and timing of application while also describing improvements in spontaneous erectile function resulting from chronic PDE5 inhibitor use (Gontero et al, 2005; Mulhall et al, 2005)

Several caveats should be addressed in considering the utility of long-term PDE5 inhibitor treatment for this clinical application. One early identified controversy was whether the therapeutic strategy could cause pharmacologically induced ‘‘tachyphylaxis,’’ as suggested by a report that described a 20% dose elevation rate and 17% discontinuation rate due to loss of efficacy in patients with ED using sildenafil ‘‘on-demand’’ over a 2-year interval (El-Galley et al, 2001). However, likely explanations for declines in treatment effect over the long term are underlying disease state progression, inadequate dosing, application of the therapy, relationship difficulties, and psychogenic factors (Steers, 2002). Furthermore, findings of consistent efficacy and tolerability of treatment following both long-term, ‘‘on-demand’’ schedules reported previously (Carson, 2003) and long-term, continuous dosing reported more recently (Porst et al, 2006; Rajfer et al, 2007) argue against the development of treatment tolerance. It is acknowledged that PDE5 expression levels apparently increase with continuous treatment in basic science experimental paradigms (Lin et al, 2003; Musicki et al, 2005a), but the consequence of increasing PDE5 expression above normative levels in the penis was not demonstrated to negatively impact physiologic erectile responses (Musicki et al, 2005a; Behr-Roussel et al, 2005).

Another matter for consideration is whether prophylactic PDE5 inhibitor therapy should be given only to patients with certain underlying medical conditions. Much interest exists to apply the therapy to patients with severe forms of ED or conditions that would predict the likely development of ED. In this vein, the therapy would apply to those individuals with such risk factors as diabetes, cardiovascular disease, prior pelvic surgery, and aging.
In their rat model study of chronic sildenafil dosing, Musicki et al (2005b) found that erections improved only in erection-impaired, aged rats but not in erection-intact, young rats. Compensatory homeostatic mechanisms were found to develop in young rats, suggesting to the investigators that such mechanisms are operable in the penis of the ‘‘healthy’’ individual in response to long-term PDE5 inhibitor treatment which limits supernormal erectogenic effects and concurrently prevents potentially harmful excessive erections.

Continued study is needed to confirm clinical impressions of a penile vascular protection benefit, which at this stage should be considered preliminary. Additionally, further investigation is needed to clarify molecular mechanisms associated with the presumed therapeutic benefit. Investigative work done in the cardiovascular field has shown the preconditioning effects of PDE5 inhibition against ischemic/reperfusion injury in the intact heart (Das et al, 2002; Kukreja, 2007). Cardioprotective effects have been related to activation of protein kinase C/extracellular signal-regulated kinase signaling, the opening of mitochondrial adenosine triphosphate-sensitive potassium channels, and attenuation of cell death resulting from necrosis and apoptosis (Kukreja, 2007). Further investigation may reveal whether or not such cellular or subcellular effects actually occur in the penis following long-term PDE5 inhibitor treatment. It is recognized that advancing the knowledge base in this area may occur most readily at the experimental animal model level, in which penile tissues are more easily obtained for molecular studies and objective erection testing is also more feasible. However, important inferences may still result from continued active research efforts expended at the clinical level. Recent work in men by Foresta et al (2007) showing that vardenafil increases circulating progenitor cells, which are involved in the process of neovascularization and continuous repair of the endothelium, via bone marrow stimulation has contributed to defining the endothelial protective role of PDE5 inhibitors.


tryhard
 

Simbarn

Active Member
lets try and keep this factual guys and not personal. If someone disagrees with another's supposition, simply state that you disagree and present the facts as to why.
There is no need to belittle or ridicule.

I tend to agree with the content in Madman's posts. I have been researching ED and it’s multitude of causes for many years now. PDE5i show promising effects with regard to the reduction of oxidative stress in our peripheral vascular system. In some instances even being possibly capable of reversing some of the damage to smooth muscle and the endothelial cells producing NO.
Excessive oxidative stress is one of the most significant causes of deterioration in the vascular tissues as we age. This is particularly evident in those with diabetes. The penis is especially vulnerable to this owing to its very high dependence on the health and function of its smooth muscle content and the sufficient availability of NO. It has been suggested that only a 15% loss of the smooth muscle content in the erectile tissues will cause erectile difficulties and this can begin as early as the third decade of life for some of us.
 

Mastodont

Active Member
So is there any reason to stick to "natural" alternatives in NO supplementation, probably some have taken daily cialis for 10 years now, one would think that possible long term adverse effects would already have occured.
 

madman

Super Moderator
It's probably mostly estrogen related. When your e2 is messed up even ed drugs do nothing.

I'd suggest trying proviron with trt and maybe doxazosin 1-2mg. I noticed benefits from HCG as well but it's not worth the e2 swings for me. With proviron and doxazosin my flaccid dick is always in "semi" state like I have just taken cialis. I used to take cialis daily but I don't recommend that to anyone anymore as you develop tolerance over years and it literally stops doing anything despite research saying otherwise. Proviron is amazing.

Guess those Italians who are at the top of their game when it comes to men's sexual health have no clue what the f**k they are talking about!

2022!





4.1.1.2 The Right Molecule for the Right Patient

The choice of the best PDE-5Is is not supported by any double or triple-blind study that compares the effectiveness of the different drugs.

This choice depends on the patient’s characteristics such as frequency of intercourse (occasional or regular use with 3 weekly or more intercourse), treatment expectations tolerability, and side effects.

In a recent meta-analysis, Chen et al demonstrated that patients affected by ED seeking immediate efficacy should start with Sildenafil 50 mg while others could benefit from Tadalafil 10 mg which has higher tolerability [25].





4.1.1.5 Non-responders

Some patients do not respond adequately to oral PDE-5Is; this mainly happens for two reasons:

1. Incorrect use of the drug
2. Lack of actual efficacy of the prescribed molecule



Regarding the incorrect use, patients must be informed about the correct intake procedure

McCullough suggests carrying out the PDE5Is treatment for at least 6/8 weeks before establishing its ineffectiveness [29]. The most frequent causes of incorrect use are as follows:


1. Failure to use an adequate dosage.

2. Lack of or inadequate sexual stimulation.

3. Search for intercourse ignoring the right timing of the drug.
In fact, there is a period of time between the intake and the pharmacological action in which the drug will be ineffective. Moreover, some patients require a longer time for the drug to start acting [30, 31].


Furthermore, the absorption of the drug can be delayed by the intake of fatty foods or a large meal.

The clinician is always required to verify that the patient has taken an official drug. Unfortunately, the black market has increased over the last decades; thus, the efficacy and safety of unauthorized and uncontrolled tablets cannot be guaranteed.

In addition to that, Marchal Escalona et al. recently reported that a polyformism of the PDE5A gene encoding the PDE-5 enzyme may affect the efficacy of the drugs. Thus, there may be variability in the clinical response of the clinical response in subjects using PDE5i [32].





4.1.1.6 On-Demand Vs Daily Treatment

Recently, there has been a great interest in daily PDE5I administration as a new and innovative approach to managing erectile dysfunction. The advantage of daily intake for the management of erectile dysfunction is the complete separation of drug use from sexual activity, eliminating the unpleasant effect indicated by patients as “I feel drugs control my sex life” or “I wish they would. my erections came more spontaneously” [33]. The main goal of ED therapy is to achieve an improvement in erectile function; however, this improvement is not the only factor for sexual satisfaction. In fact, self-confidence and spontaneity of erection may play an important role in increasing the general satisfaction of patients [34]. In this regard, a study observed that patients who started ED treatment with tadalafil once a day (OaD) reported greater improvement in self-esteem and sexual spontaneity than patients who started treatment with sildenafil on-demand. On the other hand, there were no significant differences between the two regarding the improvement of IIEF-EF, orgasmic function, the domains of general satisfaction, and of the EDITS score [35].

Regarding tolerability, it is important to emphasize that chronic administration of tadalafil does not appear to result in up-regulation of PDE5 in human penile tissue, an effect which has been observed in rat penile tissue continuously exposed to high doses of sildenafil [36, 37]. This means that the phenomenon of tachyphylaxis occurs against sildenafil and over time, the drug loses its effectiveness since more PDE5 enzymes are produced and the concentration of the drug is no longer sufficient to ensure its inhibition. On the other hand, tadalafil does not seem to show a loss of its efficacy over time due to tachyphylaxis. An additional benefit of tadalafil OaD is that overall drug exposure can be reduced in men who engage in sexual intercourse more than twice a week, and side effects can be minimized in men who have difficulty tolerating higher doses of PDE5I [33, 38]

The SURE multicenter study was one of the first trials to investigate the usefulness of chronic tadalafil dosing: 4262 men with ED were treated with 20 mg of tadalafil three times per week or 20 mg on-demand in a 12-day cross-over project [39]. The results of this study showed that over 60% of men in both arms of the study reported normalization of erectile function. Over 70% of men in both groups reported being able to successfully penetrate and complete intercourse. There were no differences in the success rate between routine and on-demand dosing for any efficacy parameter. There was a substantial difference in the timing of intercourse between the treatment arms: within 4 h of taking the drug, 53% of the on-demand arm attempted intercourse while only 29% of the OaD arm attempted intercourse within this time limit. This suggests greater flexibility in the OaD group. Although efficacy data showed no differences, the three-times-weekly dosing regimen for tadalafil was preferred by only 43% of enrolled patients; therefore, on-demand therapy was preferred by most men. Anyway, in the SURE study, it is evident that routine dosing may be a good option too.

The impact of daily tadalafil dosage on female partner satisfaction with sexual activity has also been a topic of recent interest and research. A partner preference study on sildenafil on-demand versus tadalafil OaD indicated that 79% of female partners preferred tadalafil OaD, citing a more relaxed approach to sexual intimacy and greater flexibility with respect to the timing of intercourse. Based on this, it can be inferred that such flexibility would be attractive to many patients’ partners [40].

However, it has to be stated that in some studies, side effects were more common at higher doses of tadalafil, but this dose-response relationship was not confirmed in all studies. In general, the incidence of these side effects decreases over time with chronic therapy [38].
 

madman

Super Moderator
It's probably mostly estrogen related. When your e2 is messed up even ed drugs do nothing.

I'd suggest trying proviron with trt and maybe doxazosin 1-2mg. I noticed benefits from HCG as well but it's not worth the e2 swings for me. With proviron and doxazosin my flaccid dick is always in "semi" state like I have just taken cialis. I used to take cialis daily but I don't recommend that to anyone anymore as you develop tolerance over years and it literally stops doing anything despite research saying otherwise. Proviron is amazing.

Better yet f**k the research then!

Look up who Dr. Mohit Khera is.







Dr. Khera specializes in male and female sexual dysfunction and has treated many men for ED over the past two decades.


17:25-18:15 (let that sink in your dome)





 
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