Really of all the people, madman is grumpy? Facepalm.
Let us know how things are going after more time.
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!
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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!
Age related ED: How to Prevent it and Manage it
Looking at some of the more recent studies it has been stated that: *No evidence has emerged concerning the development of any form of dependence or tolerance with the chronic use of PDE5 inhibitors. Aging-related erectile dysfunction—a potential mechanism to halt or delay its onset Monica...
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
To anyone taking Cialis daily — did you develop a dependence on it?
Anyone been on Cialis for extended periods of time to comment on whether they became dependent on it? Granted if you had ED before taking it and it fixed it for you then I can see that being some form of dependence, but I’m mainly interested in people or anecdotes of others that have taken it...
post #6
Targeting of PDE5 for Preservation of Penile Health
Molecular Pharmacotherapeutic Review Targeting of PDE5 for Preservation of Penile Health (2008) ARTHUR L. BURNETT ABSTRACT The molecular science of erection physiology has established that phosphodiesterase 5 (PDE5) serves an important biological role in the penis. Current research in the...
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.
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