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Chemical PE: The Long Awaited Evidence

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Originally Posted by london100
Today I paid $20 for an online consultation with a urologist. I tried to ask for his opinion about all this. He closed the chat window and refused to talk to me.

If anyone is currently under the care of a professional urologist they could potentially print the first page of this thread out and show it to them.

It would be excellent to get a professional opinion.

It would help all of us, not just people interested in CPE.


If urologists were remotely thinking that erection drugs could make your penis bigger, you would find them selling their ‘penis enlargement programs’ anywhere.

Ever heard of enzyte?

“they are getting back what they had lost, they are not growing bigger than before.”

Not necessarily, according to “Sildenafil Preserves…”

“At higher doses post-RRP sildenafil may increase SM content.”
The guys who took a lot of viagra went from (I think) roughly 49% SM to 56.85% SM.
That is a small increase on what they had before.

There appears to be a consensus that Papaverine is very nasty stuff. The side effects of PGE appear to be quite modest:

“The other two groups [PGE and saline] showed only minimal histologic changes or none.”
“only elongation to tumescence was found in the PGE1 group, even with double dosage”

The monkey died from exposure to anesthetic.

I admit that 24 years is a long time, but I doubt that he imagined the increase in length and girth. What you are suggesting is that he is delusional and imagined monkeys with larger penises than before. He still holds a research position at a university. I doubt that he is insane.

“If urologists were remotely thinking that erection drugs could make your penis bigger, you would find them selling their ‘penis enlargement programs’ anywhere”

That is a fair point. But it is a bit like saying: “If PE worked all men would have massive dicks”.

This is extremely interesting information:

“hypertrophy of smooth muscle were noted in the PGE1 group.”

You are obstinate, aren’t you?
“Materials and Methods: A total of 40 potent volunteers with prostate cancer underwent RRP
and were divided into 2 treatment groups, namely 1—50 mg sildenafil and 2—100 mg sildenafil
every other night for 6 months beginning the day of catheter removal.
….
Conclusions: Early use of sildenafil after RRP may preserve intracorporeal SM content. At
higher doses post-RRP sildenafil may increase SM content. The effect on the return of potency is
not known but maintaining the pro-erectile ultrastructure is integral to rehabilitating post-RRP
erectile function.

preserve

That’s why 1/5 had a diminution in SM content. They weren’t healthy guys.

‘That is a fair point. But it is a bit like saying: “If PE worked all men would have massive dicks”.’
No it’s not. To achieve a big dick through PE you have to work more than without PE; to earn more as urologists, if CPE worked, they should work the same or even less then they are doing nowadays that they know that CPE doesn’t work. But I’m sure you can find a less than honest urologist that will sell his snake oil at high price, since this seems to be your biggest desire. What Barnum used to say?

I am extremely obstinate.

The group 2 guys ended up with 56.85% SM.
The average for a healthy man is apparently 49%.
So they actually did experience SM growth despite undergoing this horrendous operation.

Barnum is widely, but erroneously, credited with coining the phrase “There’s a sucker born every minute.”

Remember I am the one actually needling my dick here.

If CPE is a sham I will go on a killing spree.

The average. That means that you can find a man with 40% and another with 60%.

You are needling your dick in the hope it will enlarge? It isn’t anymore obstination at this point.

I am not totally sure, but I think that the pre-operative content in group 2 was 42.82%

If I am correct then they went from roughly 43% to 57% despite having to go through the operation.

Obstinacy is the best quality a person can have.

Pre-operative still where ill people. I don’t know how to explain again.

Hey London, you agreed that androgens aren’t going to enlarge your penis, right?

Now, look at this: what you are believing erection drugs can do, is done way more extensively by androgens. Testosterone supplementation not only increase smooth muscle in people with ED, but also many other grow factors - see here for example:

“The androgen-dependent loss of erectile response is restored by androgen administration but not by administration of PDE5 inhibitors alone. These data suggest that androgens regulate trabecular smooth muscle growth and connective tissue protein synthesis in the corpus cavernosum. Further, androgens may stimulate differentiation of progenitor cells into smooth muscle cells and inhibit their differentiation into adipocytes. Thus, we conclude that androgens exert a direct effect on penile tissue to maintain erectile function and that androgen-deficiency produces a metabolic and structural imbalance in the corpus cavernosum, resulting in venous leakage and erectile dysfunction.”
http://onlinelibrary.wiley.com/doi/…hly+maintenance

or this
Androgens Play a Pivotal Role in Maintaining Penile Tissue Architecture and Erection: A Review
ABDULMAGED M. TRAISH
http://www.andrologyjournal.org/cgi…t/full/30/4/363

Now, if androgens aren’t going to enlarge the penis of a healthy male, how could erection drugs, with a way more limited field of action, enlarge your penis?

That is a good point.

I don’t want to be overly argumentative, but I think that there’s good evidence that long-term chronic use of PDEF5 inhibitors can actually increase SM content beyond what is normal. This is my interpretation of the “preserve” article:

Healthy men have SM content of ~49%
They get impotence as a result of prostate cancer and end up with SM content of ~43%
They take chronic daily doses of viagra for several months and end up with ~57%

You claimed that the men in group 2 probably had SM contents of roughly 57% to start with. This is possible, but unlikely:

“Published reports suggest that the
average intracorporeal smooth muscle percent is between
40% and 50%”

So the guys in group 2 probably ended up with more SM than they had before. The implication of this (IMO) is that a guy who is not impotent, who puts himself on a chronic dosage of viagra for several months would probably end up with higher SM content.

Testosterone derivatives can apparently increase SM content in people with clinically low testosterone. If you could point to evidence that testosterone derivatives can increase SM content *beyond what is normal* that would be a major blow to my argument. It would strongly suggest that increasing SM content has nothing to do with dick size.

I would say that I am 99% shore that Androgens cannot increase dick size.
The study that was posted by CYA at 8 provided pretty conclusive evidence.
It is vaguely possible that there is some sort of synergistic effect.

BTW, I was going to write “yeah but the rats were only exposed for ten days”
Then I looked it up:
Average rat life span ~ 2.5 years
Average human life span ~ 67 years
One rat day ~ 27 human days
Ten rat days ~ nearly a human year
So basically the study suggests that applying a Test derivative to your dick for nearly a year will do nothing

Originally Posted by london100
That is a good point.

I don’t want to be overly argumentative, but I think that there’s good evidence that long-term chronic use of PDEF5 inhibitors can actually increase SM content beyond what is normal. This is my interpretation of the “preserve” article:

Healthy men have SM content of ~49%
……..


“A total of 40 potent volunteers with prostate cancer underwent RRP
and were divided into 2 treatment groups,
namely 1—50 mg sildenafil and 2—100 mg sildenafil
every other night for 6 months beginning the day of catheter removal. Percutaneous biopsy was
performed using general anesthesia prior to incision for RRP. Another biopsy was performed
using local anesthesia 6 months later. Volunteers were excluded prior to the second biopsy if they
discontinued sildenafil. Biopsies were stained for SM and connective tissue, and analyzed by
computer in at least 15 different fields. The paired Student t test was used for statistical analysis.
Results: A total of 11 patients in group 1 and 10 in group 2 underwent the second biopsy.
……………….

Any conclusion suggesting a therapeutic or rehabilitative effect of early sildenafil use after radical prostatectomy
is unwarranted due to our small sample size and tissue heterogeneity.

……..

Pfizer Pharmaceuticals, Inc. provided all study medication.

http://scholar.google.it/scholar_ur…d=0CCAQgAMoADAA

:rolleyes:

‘I don’t want to be overly argumentative’ is going to win some prize.

OK, fair enough.

That just means that neither of us are right because the results are inconclusive.

Really? I do have a pill for you buddy:

“Vacuum Erectile Device

……In an early prospective study, patients were started on daily use of VED, biweekly injection of combined PGE, papaverine, and phentolamine (Trimix), and patient-directed use of PDE5-Is following unilateral nerve-sparing RP with or without sural grafting. Patients were evaluated preoperatively, 6 weeks postoperatively, and at 4 month intervals thereafter for up to 2 years for rehabilitation regimen compliance and penile length. At 4 months, only the patients with good VED compliance had a 0.4-cm increase n penile length vs 0.3-cm decrease in length in patients with poor VED compliance relative to their 6 week measurement. No beneficial effect was found for patients using ICI* regarding the recovery of penile length [45].

The follow-up study in this cohort demonstrated impressive recovery of erectile function (over 71%) that was attributed to the penile rehabilitation [46]. This finding clearly needs to be studied in a larger trial. The compliance with the rehabilitation regimen was also studied in these patients. In total, 73.3%, 66.7%, and 47.1% of patients were using VED for rehabilitation as prescribed at 4-, 8-, and 12-month follow-ups, which was significantly higher than the compliance to ICI as mentioned previously. Interestingly, the compliance was better in patients older than 57 years than that in those who were younger. This factor highlights the need to counsel all patients about treatment compliance, but especially younger men who may be more likely to neglect therapy [42].
………..
Another advantage of the VED is to ensure multiple erections on a daily basis. The average man obtains three to six erections per night during the rapid-eye-movement sleep. We do not know how many erections at a given time are required to maintain the health of erectile tissue. Therefore, the number of erections required per week for penile rehabilitation is not known. Use of VED as a rehabilitation modality can maximize the number of erections that other current rehabilitation methods cannot reach.
…..”

http://rejoynmedical.com/articles/p…bilitation.html
*ICI = intracavernosal injections

What this say to you? What is effective to increase penile size?

Does not end here. From the same source:
”. ………….Bosshardt et al. [48] used blood gas analysis to evaluate the origins of blood for erection with the use of VED. Blood gas analyses were obtained from the corpora cavernosa with VED-induced erection immediately after application of constriction ring. The measurements were repeated 15 and 30 minutes later with the constriction ring in place. The blood gas results of the corpora cavernosa were compared with the arterial blood from arterial radialis and venous blood from vena cubiti. The result showed that mean O2 saturation of corporeal blood immediately after VED induced erection was 79.2%, compared with 94.5% from arteries and 54.7% from veins. They calculated that 58% of blood with VED-induced erection was arterial and 42% of blood was venous in origin
…”

“….PDE-V inhibitors do not increase blood flow to the flaccid penis. …..”
http://www.andrologyjournal.org/cgi…t/full/30/4/384

Even more:
“………..In contrast, Montorsi et al (2008) recently reported on a vardenafil trial after bilateral NSRRP. In this randomized, double-blind, double-dummy, multicenter, parallel group study, a total of 628 men were randomized to placebo, nightly vardenafil, or on-demand vardenafil for 9 months, followed by a 2-month washout period, and an optional 2-month open-label period.

No statistically significant differences were observed among treatment groups in the proportion of patients with an IIEF EF score of ≥22 or in Sexual Encounter Profile, question 3. success rates after the washout period. Although on-demand dosing was efficacious, nightly vardenafil for the purpose of penile rehabilitation was not efficacious. This well-designed study provides a cautionary note for the present enthusiasm of oral PDE-V inhibitors for penile rehabilitation therapy.
(same source).

;)

“At 4 months, only the patients with good VED compliance had a 0.4-cm increase in penile length vs 0.3-cm decrease in length in patients with poor VED compliance relative to their 6 week measurement. No beneficial effect was found for patients using ICI* regarding the recovery of penile length.”

That is actually quite a blow to my argument. However, the VED guys were treated daily and the Trimix guys were treated biweekly. The VED guys got 3.5 times more treatment. It was not a like-for-like comparison.

“Although on-demand dosing was efficacious, nightly vardenafil for the purpose of penile rehabilitation was not efficacious. This well-designed study provides a cautionary note for the present enthusiasm of oral PDE-V inhibitors for penile rehabilitation therapy.”

That does not disprove the theory that PDE5 inhibitors can help with penile rehabilitation. There is a major debate going on at the moment about the efficacy of this technique. It remains standard practice to give patients Viagra postoperatively for this purpose, but there are some researchers who say that it will not work.

“Does Viagra work for penile rehabilitation?”
Is not the same as asking:
“Does chronic long-term use of Viagra cause increases in SM content in normal people?”
I still think that there is fairly strong evidence that it does.

I was just thinking about the implications of this argument that we’re having:

I think that its possible that (a) having an abnormally high number of erections can boost SM content and (b) this will increase the size of your dick.
I am throwing this out as a possible interpretation of the stuff I’ve read whilst arguing with you on this thread. This is just one possible interpretation.

If its true then all that is required for PE is to be hard for an abnormally large percentage of the day.
A normal person is just hard during sex/masturbation + REM sleep.
If you were hard for like 12 hours of the day, perhaps that would lead to significant growth

Someone who wanted to try this could take a nightly dose of Viagra before sleep and complete numerous short and gentle pumping sessions during the day.

That might sound a bit crazy (its just an idea)

This thread has got me thinking about PE in general and what actually causes growth. Surely it must be one of the following:

(a) Smooth muscle hypertrophy/hyperplasia brought on by oxidization
(b) Smooth muscle hypertrophy/hyperplasia brought on by a natural injury-repair response
(c) Plastic deformation of the tunica

I’d like to hear your thoughts on what you believe is the mechanism at work.


Last edited by london100 : 03-01-2012 at .

Err…oxidization?

For now, what is sure is that natural PE increase penis size, chemical PE does not.

Increase the size of tunica and smooth muscle will inflate more. There is no need of more smooth muscle, in healthy subjects, to have a bigger penis size, as the studies posted back are showing. CC are like balloons - the more blood you will push inside, the more the balloon will expand, assuming the constrictive force of TA allows such expansion.

We could speculate that a very big increase in TA size couldn’t be filled without growing more smooth muscle; but again, in a healthy subject smooth muscle will increase spontaneously. Girth work will carry more oxygen to the penis; some of the smooth muscle probably will be damaged by the unusual pressure, then repaired - so you have more smooth muscle, if needed.

Oxygenation per se can’t be enough to generate increase in penis size. It is a condition required to avoid smooth muscle degeneration, so ED. Those who have worked length extensively do know pretty well that the size of their penis can increase while EQ decrease.

Adversely, smooth muscle will always have less force than TA - otherwise you could have a broken penis just having a raging boner. No one has ever reported proofs of gains through edging. This says that, in the normal case, erection doesn’t generate enough force to increase the size of the penis. You have to apply more force than smooth muscle can generate - with your hands or a pump or a clamp.

i meant oxygenation not “oxidization”

Ahaha, for a moment I thought I was missing something.

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