Thoughts on PE from johndough

Believe it or not, your mom had it tattooed on the back of your head.

Oh I thought she had a butterfly tattooed on the bottom of her spine. :-p

I think one of the issues is that one of the tissue types that we are dealing with is poorly understood by science in general. This tissue being fascia. This is generally the tissue being talked about when anyone mentions soft tissue manipulation, and damage to the fascial tissue often is the cause of visable evidence of an accident many years on eg limps and reduced joint motion. However the range of structural differences in fascia across the body is enormous, and the commonality was previously unrecognised.

I only came across the importance of fascia about 10 year ago, when I was introduced to the work of Dr Ida Rolfe. I’m now being taught about fascia as part of my martial arts training. But still, my understanding is low, firegoat is probably one of the few people here who would have a handle on this.

Here is a nice little article.

General recommendations for working with fascial manipulation are water, cod liver oil and proteolytic enzymes (this breaks down previously formed scar tissue which hinders efforts).

People talk about muscle and bone forming the structural element of the body, but it’s really fascia. The muscle moves us, the bone gives the muscle a leverage point, and the fascia gives us shape and structure.

Redbear, I understand your point that increasing the sample size will increase the power of the study, but I don’t think we can draw conclusions about possible hidden effects without more information form the study. What was the p-value for the study? They didn’t post it in the abstract as they usually don’t if the findings were non-significant. However, if you can dig up the full article and post the p-value we can take a look at it and indeed determine if it is close enough to to what was set by the confidence interval (assuming standard 95%) to conclude that a hidden effect is possible. I think the pump protocol can be debated, I think the protocol was established based on what the researchers felt was a safe balance. I do not think compliance was an issue for most because if someone is volunteering for an opportunity to enlarge their penis with consent and medical support I doubt they would be non-compliant. I disagree that six months is not enough time to see an effect, six months is a considerable amount of time to not gain more than .1 inches, I feel this way even given the protocol used. The other study used a protocol similar to Avocet’s in that it did two 10 minute sessions per day everyday. The researchers state “The improvement in penile length is an encouraging feature and would fit with the
improvement in the curvature that was achieved.” It was also noted that those with soft plaques gained more often than those with hard plaques, it appears to me that the researchers are attributing the length gains to curvature correction.

What is the p-value? Dude, statistics isn’t going to help you much in life! LOL! Focus on what you want out of life and then go for it. You try to fit everything into the B.S. you’re learning in school man!

Thanks for posting this study Redbear, I would really like to read the full article. I was under the impression that megalophallus had a number of case studies linking it to priapism, but in general it was not a common sequela of that complication. I may be wrong and would like to see what the study says in regards to its rate of occurrence. Anyone have a link?
Also, what I would be questioning too is whether the increase in size also translated to erect size or this was simply a loss in elasticity and the flaccid was permanently deformed as the penis lost a large amount of its retractile ability. In addition, how was erection strength effect? The researchers state sexual function was retained, but to what degree? I suspect the latter question won’t be clearly answered even by that particular study.

In the mean time, here are some studies related to penile hypoxia. I’m including these because severe hypoxia is one of the damaging results of priapism. The first links lowered oxygen levels in the corpora cavernosa to the onset of erectile dysfunction http://www.andr ologyjournal.or … t/full/28/2/223
This study helps explain why pumps improve erection quality for those with ED by introducing more oxygen rich blood into the penis on a regular basis. Which also explains why regular sex/masturbation (not overdoing it) or at least obtaining regular erections is important in maintaining penile function. I think an important question to ask is how does clamping effect erectile function in the long run as it also induces acute temporary hypoxia? I’m not sure we can completely draw conclusions just yet, I think more needs to be read before then, but its important to note that it is commonly reported that clamping sessions can temporarily effect quality and ability to obtain an erection.

Next study related to penile hypoxia and its effect on endothelin (an endogenous vasoconstrictor) details some of the regulatory mechanisms in the flaccid state. I only glanced over this one as it is getting late and I am tired and have to get up early. However, from what I gathered is that the flaccid state induces mild hypoxia (those with ED experience a more pronounced penile hypoxia), which activates various chemical pathways that in a 24 hour cycle lead to a chemically induced erection (hence nocturnal erections). I can’t tie this particular study directly to PE just yet, but when I read it I will be able to.
http://molehr.o xfordjournals.o … t/9/12/765.full

I’m tired, I will reply to everyone else’s post tomorrow.

Don’t you think that even if hypoxia leads to temporary ED, the changes(angiogenesis) will make your EQ better in the long run if you rest enough and also give you a bigger penis, based on the new blood vessels forming(as I recall this is an effect of hypoxia) ?

I found this quote from that article interesting:

"Sex‐related and unrelated (nocturnal) erections are proposed to have a protective role on the trabecular tissue, by increasing tissue oxygenation and NO synthesis and decreasing pro‐fibrotic factors, such as TGF‐β1. Hence, there is the concept that ‘erections may be good for preserving erections’ (Moreland, 1998)."

I looked at the Moreland abstract and he writes,

"Correlations between animal models of disease as well as clinical reports are presented in support of a role for hypoxemia in penile fibrosis. A case is presented for a biological basis of nocturnal penile tumescence in the preservation of potency and an overall hypothesis for the molecular pathology of erectile dysfunction is proposed."

So I guess this is a good argument for getting night wood. I actually find that PEing did increase my incidence of night/morning wood.

Also maybe some level of hypoxia (not too much or it will lead to cell death) to the erect penis may act as a signal for growth (e.g. clamping). Muscle growth kinda works like that. In fact, vascular occlusion in a number of studies acts like artificially-induced muscular actions that have been shown to lead to muscle growth. A number of such studies were posted here. For example this thread:

Theory-Stimuli for skeletal muscle growth-does it apply to penis

I’m not sure skeletal muscle hypertophy could be a viable mechanism for enlargement because the extensibility and volume of the CC is the determinant in erection size. The muscle tissues act to constrict the vessels to entrap blood and to aid in ejaculation.

This article shows the ED rates following priaprism including those of shorter duration.
http://www.meds … rticle/512953_3

This is taken from another thread and was posted by penissmith /forum/printthr … 95&page=5&pp=15

Megalophallus has been previously reported,[2] but it is not generally recognized as a sequela of priapism. In our patient, this complication developed immediately after a prolonged and intense episode of priapism 9 years before the patient presented to us. This sequela did not interfere with subsequent erections. Fibrosis of the corpora cavernosa, as previously hypothesized, [2] should result in low flow by Doppler imaging. The reverse was true in our patient.

We propose an alternative mechanism for this sequela. The increase in penile circumference follows a sudden and permanent loss of elasticity of the tunica albuginea, brought about by a particularly intense priapism and a very engorged organ. The loss of elasticity of the tunica albuginea releases constraints on the corpora cavernosa, which then expand like a sponge. This expansion, helped by some subtunical venous impairment that is secondary to the remaining elasticity of the stretched tunica, results in pooled, deoxygenated blood in the corpora cavernosa consistent with our BOLD-MRI findings. BOLD-MRI defines the presence of deoxygenated blood, eliminating the need for an invasive procedure.

The plausibility of this mechanism for megalophallus is supported by the lack of increase in the circumference of the glans in our patient and the one previously described. The glans penis sinusoids are larger and the tunica albuginea is absent, and thus do not provide the bases for the pathologic features observed. The decreased elastic compression of the tunica explains the lack of pain despite the enlargement of the penis. The residual elastic restraint to expansion produces moderate blood stasis, explaining our BOLD-MRI findings. Finally, conservation of the capacity for full erection is due to the intactness of the corpora cavernosa and the infratunica venule system."

1) Megaphallus developed immediately after a long and intense priapism.

2) The size of the glans didn’t increase.

3) The pooled blood strongly suggests that the tunica is permanently expanded.

If there was massive cell growth of the smooth muscle, it would take awhile to develop and the glans should have grown as well.

So what I am seeing so far from the evidence is that priapism in most cases does not cause megalophalus. The rates of ED following even a relatively minor episode of priapism are a shocking 1 in 4. Also, it does appear the tunica is being stretched permanently; however, I do not view this as a good thing. The loss in elasticity is going to be followed by a loss in some erectile function even if sexual function remains intact. This means that your penis may get larger, but it will also get spongier as the restricting limits of the tunica would be destroyed by the priapism. The restricting factors of the tunica are what makes an erection hard as the elastic forces pull back on the CC as it tries to expand.

I had the same procedure. I gained 3/4” in NBPEL with the help of post op hanging. I hope this helps too.

I’ve got a friend who has sickle cell and he had a priapism that led to megalophalus and he is very pleased.

Hey JohnD, have you read this two threads?

Science of PE Posts and Threads. Link Here!
Loading, lengthening, healing.
Possible reason for PE induced growth

There is a good amount of articles. Most of the articles you are commenting were already posted here, with various comments, some from Physicians, just saying. We do have a good amount of brain in this site. :)

Marinera, thanks for the links. There is a lot of information in those with a lot of good studies. So far what I have read I will list below and comment on what I found.

Chemical PE
I do not think this is possible based on the studies and anecdotal reports. The different variations I read ranged from supplementation of androgens such as testosterone, HGH, to vasodilators. Testosterone and other androgens are the most widely documented in the literature. In adolescence or in cases of hypogonadism androgens have been shown to increase penis size. However, conflicting evidence in the literature shows that early exposure to exogenous testosterone may limit penis size in adulthood. Normal post puberty males have not been shown to experience an increase in penis size following exogenous androgen supplementation. This is why bodybuilders do not have excessively large penises relative to the rest of the population. I did not see a sufficient amount of information on HGH based on what you linked, not many people provided links to studies. They may not exist or maybe no one has taken the time. I particularly don’t find it worthwhile because of the cost, possible legality of HGH, and risk for increasing the chances causes abnormal cell proliferation. Vasodilators such as those used in Dr. Adam’s protocol have not been shown even the anecdotal cases to increase penis size. Stagestop followed Dr. Adam’s protocol along with supplementing with testosterone and appears to be one of the few to declare success with this protocol. Given the inability to replicate these results in others in anecdotal cases and no evidence in the medical literature showing the same vasodilator, and others similar to what was used in the protocol these drugs, can increase penis size despite being used regularly by men with ED and occasionally by men with normal penile function. Considering Stagestop’s age (50+) I would attribute his gains to an increase in erection quality in response to the testosterone or the vasodilators or a combination thereof.
Conclusion, chemical PE does not work to increase penis size, but can improve erection quality in men with low testosterone levels.