Loading, lengthening, healing.

Hi marinera,

Thanks for all the work you do in presenting these research studies!

I don’t follow this.

They say the initial examination was after the 1st episode when he was 17. Subsequent to that he had excessive growth, but he also had another 61 episodes of priapism.

I don’t see why it reads that there was a delay between stress and growth?

This bit might be interesting: “During an episode of priapism, the penis further increased in size and got very tender.”. I wonder how they measured the “increase in size”?

Hi awstev. First episode of priapism was at the age of 17; subsequently, he had other 62 more episodes, and at the age of 24yo he revelead clear signs of hypertrophy.

Also here:
“...This episode of priapism was associated with
vaso-occlusive crisis. In conjunction with pediatric
service, he was successfully managed by exchangetransfusion
using five units of whole blood. No surgical
procedure was performed for priapism.However, subsequently the penis
gradually showed excessive growth..”

He was examined for years before showing signs of hypertophy. This also seems to suggest that not all episodes had the same hypertophic effects.

Also, in the introduction of the article:
“….over a period of time, his penis hypertrophied.”

This all seems to means that there wasn’t an instantaneous growth, but this growth occured over the course of years.

This case also recall another case of megalophallus:
“For several years he utilized this apparatus when he appeared in the ring; but frequently when performing his gyrations the organ would become twisted, causing pain, tenderness, and swelling, lasting for several days, followed by a subsidence to his normal condition.

After using the apparatus for the space of two years he observed that the organ was increasing greatly in size. This condition was unaccompanied by pain.
……
The length of the organ from the pubis to the end of the prepuce was ten and one-half inches; the circumference at the middle of the body was nine and three-quarters inches .”
Hypertrophy Of Penis

In both case we don’t see a pathological or traumatic event with subsequent immediate growth, but instead an illness that caused slow and gradual growth.

Marinera, you are extremely intelligent with all of these topics. It however is a little over my head! I was wondering if we came to a simple conclusion and maybe closer to possibly gaining, from this very long thread?

I’ve heard this a number of times, but its a faulty comparison.

How do they do this?
“In the most common procedure, the tibia and fibula bones of both lower legs are broken and an external fixator device is attached to each half of each severed bone. The device is attached to the bones using pins or wires that go through small holes drilled through the patient's skin.” And, how about this?

“Also called Distraction, this phase begins about a week after surgery and continues over the next two to three months, depenmding on how much lengthening is desired. The fixator device is lengthened, increasing the distance between both halves of each bone. New bone growth occurs in the space in between. The lengthening is applied slowly, about 1mm a day. Typically a screw is turned four times a day to achieve the 1mm per day separation. External fixator devices may also be motorized to achieve continuous lengthening throughout the process. Patients should be scheduled for one to two hours of therapy each day during lengthening. By the end of this phase, the lower legs have been increased two to three inches.
The patient is generally confined to a wheelchair during the Lengthening phase and must not bear any weight on the growing bone….

Strengthening
This phase may also be called the Consolidation phase. For the following three to six months, the patient continues to use a wheelchair until the newly grown bone is strong enough to bear the patient's weight.”

As you can see, this is a hellish, grueling process…and is nothing like PE.

I can only rephrase your statement - meaning, if you think the penis has anything in common with the leg, then I don’t know what to say.

The leg is comprised of bone, tendons, ligaments & striated skeletal muscle; the penis has no bone or striated skeletal muscle.

The penis contains spongy, expansive blood-pooling tissues - which can cause it to expand in size by as much as 2-3x normal; can’t say that about the leg.

Come on marinera, how can you possibly take that seriously? That shit was published in January 1875! It’s only outdated by 134 years. Why not publish “remedies” that include blood-letting - either by directed incisions or leeches? If you go back far enough, you’ll learn that all ailments are caused by an imbalance of the body’s “humors.”

He is so misusing the term “hypertrophy” that its utterly laughable. And, as that (far more) recent PDF stated [which I included in my PDF], megalophallus has nothing even remotely to do with “hypertrophy” - it results from a “…sudden loss of elasiticty of the tunica….” :) You might say, a dramatic EtP transference.

I’m not taking for serious his use of the term hypertrophy, Wad, I’m taking for serious a story, so facts.There are photos of that megalophallus, also, and Photoshop was not invented at that time.

Thank you iron.

This thread has become my repository for studies that, even if not directly referring to the penis, could anyway have some interest for PE. Direct translations into practical work are hard, considering that some of those studies seems to say contradictory things.

So said, I think some pratical application could be drawed. One of those, is the idea of the 2-phase cycle.

In the first phase, the goal are gains obtained acting on th visco-elastic properties of the connective tissue. This is better done with low [loads x long time] work.This kind of work doesn’t cause real growth; this means that in your penis there isn’t a significative amont of new matter, if it’s cleat what I mean.

In the 2d phase, one should cause some degree of inflamation and break some fibers of CT; the consequence is that the amount of matter in the penis augments when those damages are repaired. This is better done with [high loads x short time] work.

When this 2d phase is done, one could restart from the first phase, and so on.

Other ideas that came basing on this studies (and other material that wasn’t posted here) are linked with these threads

Overloading Fatigue Experiment

Clamping: Advanced Empirical Discussion

(for which, of course, most of the credit is due to our fellow Long Vehicle).

I was forgetting this part. The recent PDF that you are referring to is this

Abstract

Priapism is a common complication of sickle cell anemia. We report a little known sequela of priapism: painless megalophallus, with significant penile enlargement. The patient had had an intense episode of priapism 9 years previously and his penis remained enlarged. Blood oxygen level-dependent magnetic resonance imaging revealed enlarged, hypoxic corpora cavernosa. Megalophallus probably resulted from permanent loss of elasticity of the tunica albuginea due to severe engorgement during the episode of priapism. This sequela needs to be recognized by physicians because no intervention is necessary and sexual function seems to remain intact.”

Para-Goomba - Megalophallus: 7.5” flaccid girth! (photo)

You see? It’s an opinion of the author, not a fact or a commonly accepted view in the scientific commnunity.

Another point:

“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.”

So, they are basing their hypothesis on the fact that the glans wasn’t hypertrophied. Now, have you read this?

“….It is interesting to note that the penile hypertrophy was

confined to the corpora cavernosa and that the glans and

the corpus spongiosum were of normal size. It is well

known that the latter structures are not involved in

priapism and hence they are not subjected to hypoxic

stimulus to under hypertrophy.”

marinera - Loading, lengthening, healing.

What it gives?

NB: you may note that I’m using the fulltext of the case study, not an abstract.

The science is intellectually interesting, but the reality is that jelqing works, stretching works, hanging works, pumping works, clamping works etc. Although there is no physiological comparison with weight training, a similar situation exists; free weights, machines, kettlebells - they all work. You can think of lots of other examples for yourself. Considering the money involved in muscle building as an industry, no one vastly superior approach has been arrived at. You see what I’m getting at?

Whatever examples you come up with, they will all have a simple common denominator: consistency over time. Nothing works if done for a few weeks then stopped, or drastically reduced. Some results will be gained, but nothing worthwhile.

Many guys want some ‘scientifically proven’ method that will give them the fastest gains, and won’t even begin PE until they have it! By the time that comes along, they could have built their penis and been on maintenance. Or they just want an ‘easy option’ - maximum results for minimum work; those guys will never succeed with PE because they don’t have enough desire to stick even with the easy option.

Even if a ‘perfect method’ is worked out (I doubt it will be - too many variables), the most vital thing will still be consistent effort over time. If guys would just work on that one thing and not worry about exactly what they were doing, there would be far more guys getting good results from PE.

After all, we all get a feel for when our penis has had ‘enough PE’, ‘too much PE’ and ‘not enough PE’. Get ‘enough’ regularly and only take a break when you have worked hard for a few months and the gains have stopped, and you will grow. It’s not ‘cutting-edge science’, but it does work.

Firegoat, - I absolutely agree with your thoughts.

On the other hand, I remember wild discussions on the theory of PE, some of which I initiated myself, and some others that I joined.

Most of the time, however, while reading others’ threads or typing my own posts I was hanging weights to combine “applied” PE with the intellectual pleasure to discuss why things work (or often enough: don’t work).

Now, although closer to may goal than when I started PE but with gains slowing down I have started to consider PE as a way of meditation. And gains are still welcome, and so are discussions on PE.

International braz j urol

Print version ISSN 1677-5538

Int. braz j urol. vol.29 no.4 Rio de Janeiro July/Aug. 2003

doi: 10.1590/S1677-55382003000400007

CASE REPORT

He was unable to ejaculate, his penis swelled, and he endured prolonged erections? And he was unable to “exteriorize” his glans? Could you translate this into PE-speak?

I encountered this case report casually while surfing on the Internet and posted here just out of couriosity, but I don’t think it says that much to us PEers.

It’s even unclear if the increase in size was just due to fluid build-up - no exams were performed out of physical examination. He was unable to ‘exteriorize his glans’ due to the skin swelling, that caused phymosis.

The only thing that could be interesting is maybe this:
>>Two years after the beginning of the rubber band usage, he observed progressive penile swelling and an incapability of exteriorizing his glans penis one year later <<

so, no continous adaptation, but at a given point, with repeated use of the cock-ring, a swelling (increase of size?) started. It recalls my idea of the point of accumulation of load.
Using a formal language, there seems to be a discontinuity point between the function : (application of load -> adaptive reponse).

I’m not sure we can derive that, it could be that the report was written in poor or inexact English (it is not in a native speaking English country). But if that were true, it’s very interesting. I could see that that might be true of lengthening procedures, but a delayed response from severe overload of girth work should be dangerous.

While he did say “probably,” I would regard it as more than a mere “armchair opinion.” Remember, they conducted a scientific study on the patient, as well as thermal imaging photography (in other words, that had quite an in-depth view of his inner penis, upon which to base their conclusion [about the loss of elasticity] - clearly they saw what they saw).

Furthermore, they indicate “This sequela (the long term after effects) needs to be recognized by physicians because no intervention is necessary and sexual function seems to remain intact.”

“…needs to be recognized by physicians….” sounds pretty damn confident.

(1) That the glans wasn’t enlarged is no surprise at all to me (we’ve had several discussions here about the difficulty of glans enlargement), and my theory is that the glans is so incredibly elastic. Regarding the CS, that is a little surprising, but not greatly. After all, most of us probably recognize that we get the majority of our girth gains from the 2 large chambers - the CC.

(2) marinera, I know that English is not your native language (and I confess that you speak it better than I speak my 2nd or 3rd language), but I think you missed something on your reading of that technical material: You said, “So, they are basing their hypothesis on the fact that the glans wasn’t hypertrophied,” but that is not accurate. They did not “base” their theory on that, they stated that “…The plausibility of this mechanism for megalophallus is supported by…”etc., etc. They merely referenced it, after the fact, as a supporting/non-contradicting observation. I don’t mean to sound like a hair-splitter, but there really is a difference. I’ll bet that much of their conclusion was “based” on their scientific tests, thermal imagery, etc. And then, summing it up, they referenced what they did about the glans & CS.

(3) I will concede that they seem to be employing a “generic” reference to hypertrophy, and not always the strict application associated with striated skeletal muscle. Because even though they claim the massive enlargement was due to “loss of elasticity,” they still employed the phrase “hypertrophy” (obviously in a loose manner). Yet the other, 134-yr old, study is far from modern science.