Chemical PE: The Long Awaited Evidence

Haters!

After 20 minutes, you have to release pressure, not remove the device. If you don’t use a constriction device and keep alternating pressure in short spans of time, you have an increase in oxygenation, not a decrease.

And yes, it’s quite adverse, because actually a prolonged erection due to ED is known to cause priapism, fibrosis and degradation of connective tissue. So, if correctly used, there is more oxygenation with vacuum pumping than with erection drugs. Beside that, a pump gives way way more flexibility and allows different protocols - something that drugs don’t allow : you make the injection and have to hope a priapic episode doesn’t begin, or you have to have blood suked of from your penis with a sirynge or take another drug and hope it will work

I’m known to be a not big fun of pumping; but I repute myself a balanced guy and there is not comparison, under about any perspective, between erection drugs and pumping: the latter beats the former from a long run.

It’s not just my profan opinion: you can read here how vacuum pumping is being re-evalued by specialists in comparison to drugs:
http://www.meds … warticle/725873

"Vacuum therapy (VT) utilizes negative pressure to distend the corporal sinusoids and to increase the blood inflow to the penis. Depending on its purpose, VT could be used as vacuum constriction device (VCD), with the aid of an external constricting ring which is placed at the base of penis to prevent blood outflow, maintaining the erection for sexual intercourse.

Also, as a vacuum erectile device (VED), without the application of a constriction ring, just increases blood oxygenation to the corpora cavernosa and for other purposes. The emerging of phosphodiesterase 5 inhibitors (PDE5I) for the treatment of erectile dysfunction (ED) eclipsed VCD as therapeutic choice for ED; however, widespread usage of VED as part of penile rehabilitation after radical prostatectomy and other purposes rekindle the interest for VT.

The underlying hypothesis is that the artificial induction of erections shortly after surgery facilitates tissue oxygenation, reducing cavernosal fibrosis in the absence of nocturnal erections, and potentially increases the likelihood of preserving erectile function. Due to its ability to draw blood into the penis regardless of nerve disturbance, VED has become the centerpiece of penile rehabilitation protocols. Herein, we reviewed the history, mechanism, application, side effects and future direction of VT in ED."

I suggest anybody to read the full (free) article, it is quite interesting. Mechanics beats chemics!

Still you are building a sky scraper on nothing. It is just your opinion, that paper and those emails don’t confirm what you think.

You don’t understand why CPE has been a failure? That says us something.

I hope you get the gains you are aiming for, but this doesn’t means I encourage dreams that are likely to become incubus. Better be know as an argumentative ass than a snake oil seller.

You make a good point.

I did a lot of pumping for a long period of time. I did experience visible length gains, though there was some retraction after I stopped pumping. I never gained any girth, which was my objective.

That is the reason I switched my attention to chem pe.

You can mitigate the risk of priapasm by keeping certain meds on hand. I have never experienced a priapasm.

I have gone through the titration stage and have given myself around a week of two hour erections. I had to give up because of lack of time and money. I will be re-starting in a few months. I used research grade pge-1 (medically filtered) and Andractim. I did not see any growth (I only did it for a week). I did not experience any negative side effects. My erectile function remains good.

CPE has not been a failure

The paper and the emails are unambiguous. They injected monkeys with papaverine and significant visible enlargement took place.

I understand that CPE is not for everyone. If you are having success with pumping then you should probably stick with that.

“Over the long term, papaverine maintains its erection-inducing capability, but it does cause pathologic changes in the erectile tissue: minimal to marked fibrosis at the injection site and hypertrophy of smooth muscle in the non-injected area of the corpus.”

This is what the article says.

And contrary to what the author of the paper guess in the email, it’s likely the lack of oxygenation that has caused hypertrophy - prolonged ischemia is known to cause smooth muscle hypertrophy; the problem is that the hypertropied tissue lose elasticity, and in the specific case of the penis, this is known as a cause of impotence.

Adversely, I’ve never heard that hyperoxygenation leads to hypertrophy of smooth muscle.

And still no measured increase in size in those monkeys. I doubt a serious scientist would say: “I think we have witnessed an increase in the size of the penis (but we didn’t thought to measure)”.

Which photografic evidence exists of successful CPE? I have to have missed. If you can point to people who are not trying to sell something and can show proof of successfull CPE, I’m all ears. As far as I can remember, even a Doctor who invested on CPE and patented a process abandoned it.

Before or after some magic pill will be discovered; but papaverine has been around for a lot of time. It is an abandoned substance for a reason. If it was able to enlarge your penis, a bunch of Pharmas and Docs would be selling it as miracolous remedy.

(1) You are clearly very knowledgeable, but with all due respect this man is a professional urologist. He is a professor and an expert in this particular field. I would tend to favour his explanation over your one.
Are you sure that hypertrophied smooth muscle tissue looses elasticity and causes ED. Could you provide a link? I would be grateful if you would.

(2) This guy is a serious scientist. He holds a professorship at a good university. The lack of measurement can be explained by the simple fact that enlargement was not something that they were looking for. To accurately measure the increase in size they would have had to take measurement before the start of the experiment. They were not originally interested in size, which is why they never did this. The fact that he is a serious scientist and claimed that there was enlargement without measuring it is a good sign. It implies that the increase was so pronounced that (in his words) it was “immediately obvious”.

(3) Photographic evidence in this context proves nothing because of photoshop programs etc. Apparently Dr. Adams is still offering chemical pe services, but only to existing clients. He is refusing to take on more patients. If you call his office he will say that he has abandoned chem pe entirely, because he does not want to lose his medical licence and/or get sued for malpractice.

(4) I am not advocating using Papaverine specifically, I’m just pointing to evidence that chronic use of an injectable ED drug will lead to growth. Anyone who wants to try this should use Caverject or Tri-mix.

If I remember correctly, the full article states that the doses remained the same. The duration of the erections did not decline. That suggests that the erectile function of the monkeys remained the same.

There were no references to a decline in erectile function in the article.

Cavernous smooth muscle hyperplasia in a rat model of hyperlipidaemia-associated erectile dysfunction.
Qiu X, Fandel TM, Lin G, Huang YC, Dai YT, Lue TF, Lin CS.

Abstract

What’s known on the subject? and what does the study add? Increased cavernous smooth muscle content has been repeatedly observed in rat models of hyperlipidaemia - associated erectile dysfunction. This study shows that the increased smooth muscle content is due to hyperplasia.
….
CONCLUSIONS:

• Hyperlipidaemia is associated with reduced nNOS-positive nerves, reduced endothelium, and increased CSM in the penis. • The increased CSM is attributable to hyperplasia. • These structural changes may explain why hyperlipidaemic men are more likely to develop ED.

Cavernous smooth muscle hyperplasia in a rat model of hyperlipidaemia-associated erectile dysfunction

I suppose you aknowledge hyperplasia and hypertrophy are often used as synonyms in the literature (although those, strictly speaking, are different processes) to mean "grown tissue".

You can also read this post and the references
marinera - Loading, lengthening, healing.

or, definitely, just google a bit. You’ll find that hypoxia -> smooth muscle increase (as much as changes, namely increased collagenous content in smooth muscle, with decreased distensivity, see this for example
http://www.meds … rticle/449624_7 ). Transferring this to the penis, what you have is that priapism (lack of oxygenation) -> smooth muscle growth/change -> erectil disfunction.

Sure. Expecially when you consider that his colleague said there was no enlargement.

3) , Dr. Adams is refraining to treat patients with CPE. In your mind this means that CPE is effective? Ok.

4) Caverject is better than papaverine for sure. If you find some serious proofs that Caverject caused measurable enlargement, post them.

You made up your brain that CPE will work, it is just that simple.

I am pleased that I have found someone to have a real argument with. You clearly know what you are talking about.

However, I think in this case you are wrong.

(A)

When you read the abstract of the first study that you posted it sounds as if having more cavernous smooth muscle (CSM) in your dick is a bad thing.

But when you read the full text it sounds as if they are actually saying the opposite:

“In the penile corpus cavernosum of these rats there were
fewer nerves and fewer endothelial cells,
which are features consistent with decreased
erectile function. However, there was also a higher cavernous smooth muscle (CSM)
content, which may indicate ***BETTER*** erectile
function.”

“Erectile dysfunction is usually associated with
a lower CSM content”

On the other hand, they do say this:

"hyperplasia in
the CSM is probably associated with less
contractility"

My interpretation of the article is this:

People with the disease Hyperlipidaemia are more likely to have ED
This disease gives you (1) reduced nNOS-positive nerves (2) reduced endothelium (3) increased CSM in the penis

(1) and (2) are bad.

(3) is usualy good, but could be bad if it makes for less contractility.

Also, I admit that hypertrophy and hyperplasia are often used synonomously, but it is possible that the two could be different in an important way. If you read the study about the monkeys they look at samples cut from the penis under a microscope and observe hypertrophy not hyperplasia.

hyperplasia may be associated with less contractility, but hypertrophy might not be.

(B)

I admit that the professor’s explanation sounded weird. Like you I assumed that the mechanism was hypoxia. His claim that the increase in size resulted from oxygenation sounds a bit fishy. I will do more reading on that and try and work out whether or not that is a stupid explanation. But I assure you that this guy is a genuine scientist. He is a professor at a prestigious university. He is one of the six authors of the paper. I will PM you his name if you are interested. I could not find the medscape article you posted, please could you state the title so that I can find it through google.

(C) Dr. Adams is still doing CPE, but only to existing clients. I am in contact with one of his current clients, who is a member of this site. Adams is trying to keep a low profile.
Caverject and papeverine are different drugs, but the principle is basically the same.

I think in fairness you should admit that there probably was significant enlargement. I don’t believe that this professor and his secretary wrote those long replies to wind me up. The professor stated that there was a significant increase in size that he did not expect and that this was visible to the untrained eye. (1) He did not measure it because that was not initially part of the experiment

(2) In the article it is recorded as an unexpected finding, which is why there were no before/after measurements

(3) The other researcher probably sensed that I wanted to know if I could increase the size of my own penis by following a similar protocol. Under those circumstances it is not surprising that he fobbed me off.

Priapasm is obviously a cause of ED.

I don’t think people who experience Priapasms get ED because of hypertrophy/hyperplasia of their CSM.

They get ED for other reasons

Cavernous smooth muscle hyperplasia in a rat model of hyperlipidaemia-associated erectile dysfunction.
Qiu X, Fandel TM, Lin G, Huang YC, Dai YT, Lue TF, Lin CS.

Don’t know why the link doesn’t work.

What I’m trying to say is that lack of oxygenation has different effects, depending on the severity and the time it lasts. Mild/not prolonged lack of oxygenation seems to promote hypertrophy of about any tissue; if the oxygenation is reduced for a very prolonged span of time, there is a turn from hypertrophy to hiperplasia (or the adverse) properly said; but these changes can be seen to be the border line: from a healty tissue to unhealty tissue; in the case of smooth muscle, it can become thicker but anelastic, because it is has lost his characteristics due to more collagen deposition; this makes the smooth muscle less distensible; if this smooth muscle is in the penis, there it starts ED.

I don’t have the time right now to retrieve the articles on which I’m basing this reconstrucion; anyway, you cound find this interesting, for example:

"Hypoxia-induced brain angiogenesis in the adult rat
Sami I. Harik*tt, Martin A. Hritz* and Joseph C. LaManna*t§

1. Prolonged hypoxia increases the brain vascularity. Here we studied the protein and
deoxyribonucleic acid (DNA) content of isolated cerebral microvessels in hypoxic and control
rats.
…..
4. The cell size index (mg protein: mg DNA) of isolated cerebral microvessels increased after
1 week of hypoxia, suggesting microvascular hypertrophy, but returned to control by the
second week of hypoxia and decreased to below control levels by the third week of hypoxia,
suggesting microvascular hyperplasia. These results indicate that the increased vascularity
of the brain in hypobaric hypoxia progresses from an early phase of microvascular hypertrophy
to later microvascular hyperplasia.
…."
http://jp.physo c.org/content/4 … _2/525.full.pdf

Back to PE: I don’t think that any attempt of CPE will result in ED, or that, theoretically speaking, there is zero chances that some limited gains can result (or more likely made easier, if hand in hand with a mechanical stimulus) from it; what I contend is that it is harder to modulate the effects of erection drugs than the effects of natural PE; neither I see any specific action of those drugs that NPE can’t achieve in a more effective and controllable way. When you add the astronomic cost, I think the chanches of having significative gains that can’t be achieved through NPE are about 1 on 1 million.

Hope I explained my point of view.

Because smooth muscle becomes anelastic, due to more collagen deposition.
http://urogenit alresearch.org/ … 14_1_4_2009.pdf

(Changes in TA tissue could be as much relevant, of course, if not more. But we are speaking of smooth muscle now.).

Smooth muscle hypertrophy is the first step, hyperplasia the second, fibrosis of smooth muscle the least. Going from one step to the next is not unavoidable, but one has to be very careful. The time needed from an organ to another, or a men to another, or even specific circumstances, can vary a lot. A 20y guy in perfect shape in a warm room maybe will not experience any harm from a 3 hours erection; a 50y, obese man, with an incipient diabetis, in cold day could report significative structural changes.

And at the bottom of this all: how increased SM can increase the size of your penis? There is little doubt that the limiting factor will be tunica albuginea. That’s why you don’t see many proofs of gains among edgers, despite all the yada yada.

I think that the difficulty in modulating chem pe has been exaggerated. I have personally found that if you get the right dose then the erection time is pretty much stable and easy to control.

I agree that NPE is infinitely preferable to actually sticking needles in your dick, which is not much fun. But NPE has not really worked for me. I have tried pumping and clamping and have failed to gain girth. That is why I have moved on to CPE.

The cost of (filtered) research grade pge-1 and Andractim is not actually very high. I have injected this several times and my EQ remains good.

I am still confused about the professor’s oxygenation theory. I will look into it at a later date.

Thanks again for your input. I need all the advice I can get.