Yet another theory of how we grow

I’m going out on a limb here. But since Wadzilla brought it up. I think a long sustained erection at 100% hastens gains. I’m talking greater than 20 minutes of jerking off without cumming. So edging practice or ballooning does not stop or hinder gains. But may actually improve them.

Any loading stress, longitudinal or circumferentially, on the tunica would put stress on the collagen fibrous elements, elastin fibers and fibroblasts themselves. I guess the question is whether when you edge or masturbate you over extend or in essence overload the tunica to the extent that you achieve when you jelq, squeeze, Uli or slinky. I would suspect not.

Ballooning with a ring, I not as sure, because the pressures exerted with in the cavernosa will exceed the 200 - 300 mmHg normally achieved in a hard erection with ishiocavernosa muscle contraction. Because of the maximal filling and very low compliant tunica at this maximum erection, pushing and retaining more blood (probably very little) would cause an almost exponential increase in cavernosa pressure. This should be a significant load stress on the tunica at least circumferentially. It would be difficult to assess its contribution to your PE successes because you already do significant girth and lengthening PE that probably cause even greater overload. I guess you can say, it couldn’t hurt.

When I started PE I could not get a full erection without jelqing first. Then once it was up there I went for it. I do believe certain ballooning practices can help in gains. Perhaps erect kegels can push the chambers to new maximums. Too early in the erect kegels routine to tell if there is any gains.

I read the definition that you posted, because I trust you:

now, I have a poor English knowledge, but I think the enunciate you referred is, said more clearly, :

<< Hyperplasia is defined as “….the abnormal multiplication OR the abnormal increase in the number
of normal cells in normal arrangement in a tissue”. So, as I said, it validate this opinion: “If we don’t believe
that penile growth from PE is (or should be) a consequence of a patologic or traumatic event, we have to
believe that, likelihood is hypertrophy the phenomenon involved in PE gains.”
But I want to take your last definition: are you saying that you are referring to hyperplasia as…” normal
increase in the number of cells..”? OK, let’s see:

So, aren’t the healing processes they are referring to, coming after a surgery and/or an injury?
Doesn’t it validate even more my hypotesis?

My Medical Encyclopedy says not all fibers are cells: some are, like muscular fibers,others aren’t, like many
connective tissue’s fiber: these are a-cellular material. Collagen fibers aren’t cells, is said here. Fibroblasts’ hyperplasia is seen after a bone ropture, but the augment of tissue is not due to new fibroblasts, but mostly to fibrosis tissue: but, of course, my book could be wrong.

In any case, fibroplasia is the formation of fibrous tissue: could this be a case of “..hyperplasia as normal
increase in the number of cells..”? Are fibrotic tissues normal cells? Your definition is very
impressive, but what I think is that we started speaking of “growth by more cells of same kind of those we
have” and you ended speaking of fibrotic tissue. However, should this means that, in your opinion, gains from
PE are due to fibrous penile-tissue formation?

Fibrous tissue growth is typical of post-traumatic/patologic states; fibrous tissue formation/growth is
associated whit loss-en functionality of the body-part. Said shortly, all source I have consider hyperplasia (properly said) a very different thing from fibroplasia; however, even if hyperplasia and fibroplasia could be considered the same (or analogues) thing,we were not speaking of hyperplasia in that sense.

What I could said? You’re a lucky and intelligent man. This doesn’t means that I can’t debate here, I hope.

Are you saying that muscles aren’t connective tissues? Or that muscle tissue is not penile tunica? But leg’s
ligs are not the same thing of penile tunica.
I think, for this discussion, muscle tissue regeneration after non-(traumatic or patologic) event is more interesting of lig’s surgery after serious injury.I think that with Pe-work we want to make our penises bigger, like BodyBuilders want, trough weight-traing work, make their muscles bigger.

Note that I’m not saying that PE-work and BB are the same thing, just that there is less difference between PE-work and BB than between PE-work and torn/ablation/illness healing process; to be clear: I think healing process, related to PE, should be called recovering process.

There are differences between how our bodyparts recover after a work (even if this work cause microtears) and how they heal after a traumatic event like a rupture; our penis has his all functionality after PE-work - not the same after it’s cutted-off or broken.

Proofs? References? Your’ abstracts are referring to this: fibrotic tissue formation after a surgery not
affecting the penile tunica; even if tunica was involved, do you think surgery on penis (after this has been
seriously damaged, I suppose) is a normal thing? When we are PE-ing we should mutilate our penis in hope that, in the healing process, fibrotic tissue will form?

You are a Doc, I’m not; but I have read what others Docs are saying, so: if you know that hyperplasia, as a
means to grow for tissues similar to penile tissues, NOT after a cut/rupture/patologic states etc.., has
be proven to happens in humans, post links/references, and I’ll be really glad.

I suppose that we all are here to know something more, not to be rewarded as “the smartest guy on the forum”, right?

This is certainly plausible. My skepticism about edging/ballooning stems from Dr Lin’s site, and is mostly reserved for those who claim “great gains” from exclusively those practices. Furthermore, Lin actually bashes jelqing & stretching as “dangerous/ineffective”; rather, he encourages only edging/ballooning - and, of course, the costly purchase of all the crap supplements he peddles.

Since the tunica cannot be “accutely” stretched (it’s too tough, and great force would only burst it), then just about anything that can apply *chronic* tension to the tunica should - in theory - be beneficial.

Isn’t it possible that both means for growth are correct? They are not mutually exclusive.

Plastic deformation in short-term growth, and biochemical growth in the long run. The degree to which each one makes your weewee grow probably would vary from person to person.

A connective tissue is a mixture of fibroblasts (cells), fibers (non-cellular; collagen, elastin, etc.) and ground substance. Most of the components of connective tissue are not cellular (also known as acellular). The fibroblast (“blast” means to build) makes all the subunits of collagen (and other fibers) that when released outside the cell and spontaneously form into fibers (through biochemical processes of proteins; namely cross-links and loose interactions). The fibroblasts build connective tissue of all types which is by definition a fibrous tissue.

By definition, acellular structures do not hypertrophy (get bigger). There may be more collagen (or other) fibers, but they are of the same structural size, not bigger.

The cells in bone that build new bone are osteobasts.

The growth in PE is believed to be through the micro injury and repair of the connective tissue of the suspensory ligaments and the tunica (to skin and blood vessels to a smaller degree).

Any process that disrupts the normal physiology or anatomical relationships are considered to be pathological or pathophysiological, no matter how small.

Disrupting or breaking fibers or links between fibers is injury.

Fibrosis is the overgrowth or reaction to severe inflammatory processes, such as interstitial fibrosis of the lung or breast fibrosis. Fibrosis is pathological, fibrous tissue is not.

Fibrotic tissue is the abnormal accumulation of fibrous tissue (the process of fibrosis).

For the reasons stated above, this is not correct.

I like to debate. I have not and will never tell you that you cannot or should not debate. It’s great to read alternative ideas.

No, muscle itself is not connective tissue. The sheaths covering them and the tendons are connective tissue.

Yes the organization of the tunica is different from the suspensory ligaments, but they are both connective tissues that heal and repair in similar manners.

Muscle growth is through increased muscle fiber size (hypertrophy), not increased cell numbers. As such, comparing the growth of muscle and connective tissue is not relevant. Again, fibers are not cells and therefore do not hypertrophy.

The medical references I’ve seen do not support this. If you find some, please share them.

It is correct that repair of minor injury versus traumatic tears, ruptures or amputations is quite different as to the result of the repair but not the manner of the repair.

There are no references that I could find specifically regarding repair of injury to the tunica. There are case reports of penis fractures (tunica rupture), but they do not concentrate on the mechanism of healing and repair.

The references I posted discuss the process of healing and repair of fibrous tissue, not fibrosis or fibrotic tissue. Just because these are published in surgical textbooks does not mean the process is different for any level of injury. However, the degree to which the injured connective tissue remodels depends on the extent and severity of the injury.

I am not “the smartest guy on the forum”. Not even close.

My goal is to share information that I can pull from the medical literature. I have access that most guys don’t have. As I said before, this information is not always available; most people either don’t dig through medical libraries or can only obtain the abstracts of publications. In many cases it takes good money ($30+) to get the whole paper. If I find information that is important to this forum, I will share it. I can assure you that when I do, I will not snow you with medical jargon to blind you with BS.

Ok, pudendum, now it’s clear where really we start seeing things in different way: you say that (safe and plain) PE work is a cause of injury (even very little injury). I think, as said, that PE work should not cause injuries, in the proper meaning of this term.

You tell me: if we are doing stretching regularly (gentle stretching, as physioterapists advice), we are producing hyperplasia in the ligs or overgrowth of fibrous tissue? Is stretching, sistematically and kindly,
tendons/ligs the same thing of using so much force to cause rupture of them and waiting for healing? Isn’t true that lig-injury will make it shorter, not longer?

I know what I see : if I have a little cut to my finger, it will disappear after few days; if my finger is cutted-of, a surgical procedure is required, my finger will not re-grow by itself. Quantitatives differences of stimulus calls for, after a certain limit, qualitatives differences in body’s reponses.

However, now your theory should be that PD happens before healing; so, I have to agree with karl: you’re a little obscure. You were saying that penile growth happens for augmentation in number of cells, now you’re saying that happens because connective tissue is over-stretched so much that it break- but, before breaking, it should reach a point were elasticity is loss-en; at this point, tunica should remain elongated.

I.E., your model (PE gains like injury-gains), should imply that, over some time under high tension, fibers will permanently elongate; a little more tension, and fibers would break. When healed, fibers of tunica will be longer/thicker.

But, if this was the case, we all knew how penile gains comes: pull your penis with so much force that it will be deformed/broken. We all know, I think, that this approach will not lead to gains.

Add to this that, as I posted before, this can’t explain gains obtained with stretchers/extenders.

I hope what I’m trying to say is clear; in case it isn’t, I apologize.

Tell me how by your model that lengthening of either the suspensory ligament or the tunica (either longitudinal or circumferential) occurs. What is causing the lengthening? Collagen fibers have a capacity to stretch but they will return to their rest length over time. The only way to get sustained effect would be through adding more subunits to make it longer.

I think that maybe we have come to an impasse here.

I’ve read something that maybe is related:

Journal of Andrology, Vol. 21, No. 3, May/June 2000
Copyright
American Society of Andrology
ReviewPeyronie’s Disease: Etiology,
Medical, and Surgical Therapy
WAYNE J. G. HELLSTROM AND TRINITY J.
BIVALACQUA
From the Department of Urology, Tulane University
School of Medicine, New Orleans, Louisiana.

Here is explicated that Peronie’s disease is a connective tissue disorder, where changes in collagen composition of tunica albuginea end in fibrous plaque containing an excessive amount of collagen, altered elastin framework and fibroplastic proliferation.

Is suggested that these changes are consequence of an infiammatorychanges of the tunica albuginea are the result of an in-flammatory process triggered by vascular trauma (Jarow
and Lowe, 1997; Carson, 1999). After a trauma or inury to the penis, cytokines is released, activating fibro-
blast proliferation; there is also production of collagen, the main extracellular
matrix component of a Peyronie’s plaque.
So Peronie’ disease has been defined as a wound-healing disorder, like the dermatologic con-
ditions of keloid formation, hypertrophic scarring, and Dupuytren’s contracture (Levine et al, 1994). …….

Even more interesting:
http://www.blac kwell-synergy.c … 0X.1997.26511.x
(free full text)

authors found that Objective To investigate whether changes in the structure of the tunica albuginea influence the development of erectile dysfunction.

Patients and methods Biopsy specimens taken from the tunica of 64 patients (both potent and impotent) with and without Peyronie’s disease were evaluated. Tissue samples were stained and examined under light and electron microscopy, and the concentration of elastic fibres present in each was measured using computerized image analysis.

Results The concentration of elastic fibres was lower in impotent than in potent patients (P=0.0365) and was also significantly less in patients with Peyronie’s disease. Furthermore, the concentration of elastic fibres decreased with age. Electron and light microscopy revealed the presence of distinct alterations in the tunica albuginea in impotent patients and patients with Peyronie’s disease that might interfere with function.

Conclusion The decrease in elastic fibre concentration and changes in microscopic features may contribute to erectile dysfunction by impairing the veno-occlusive function of the tunica

it’s a beatyful article, with photos of micro-structure of tunica and lot of information. In the core of article is explicated that the elastic fibers were disordered and bundles of collagen were separated and dispersed in most of impotent subjects.

Basing on this :

1. fibroblasts proliferation is supposed to be (one of?) the mechanism trough tunica albuginea could heal/grow;
2. loss-en of elasticity is a cause of impotence.

We have to add:
3. elasticity of penile tunica diminish with age (even in non-impotent males).

Let’s hazard:

a) PE-work act stretching the penis, in length or girth direction is the same for our purpose;
b) if this stress is prolonged for a given amount of time, tunica start loosing elasticity:
that’s why many believe that longer FL after stretching is good sign, and clampers say that after a good session penis is fatter for hours or days.
c)this reduction in elasticity could explicate why after too much PE-work somebody experience ED and/or augmented urinary frequency;
d)the reduction in elasticity is the signal for the body to start new "meat" production (new elastic fibers and/or
new collagen and/or new fibroblasts);
e) after the process sub d), tunica become more elastic and Erection Quality is better.
f) newbie gains could be a consequence of inversion of the elasticity loss-en process.
g) if stress is too much intense/prolonged, fibrotic tissue could be produced in the penis, that will reduce future gains, ED and nerve damage (given the protecting function of tunica)- so, it should be wise to take at least 1-2 days a week to rest.
g)this accord also to PI’ theory, by sparkyx et al..

In someway, both PD and new tissues progressive formation could concur, at difference stages, to explain PE gains.

Given the structure of tunica, more complex than commonly believed, it’s also reasonable that even a submaximal elongation of penis, if sufficient prolonged, can lead to gains, as reported by extenders users.

What you, science-minded guys, think about?

DR. Linn does not know his ding dong from a door bell, but constant tension applied to the tunica would seem plausible. The tunica I think like other members of the penis can be softened through warm up. Jelq first thern go into a edging session seems like that may be the key to some gains.

Or hmm, the tissues and matrix of the tunica itself can grow, It happens with jelqing although very stubbornly. Again softening it up with heat.

My question is is the same tough fibrous tissue that composes the tunica the near same material as the ligs?

Kingpole - I think the following comparison with a joint would hold:

Lig of joint = lig if dick
Capsule of joint = tunica of dick

If that is so (and I believe that this is the case) then both are practically identical. Ligs are simply a local thickening of the capsule / tunica.

Then perhaps something like glucosamine/chondroiten may be useful in pecker hypertrophy in the ligs and tunica.
And for the smooth muscle, blood vessels and other cellular bodies something that would trigger growth here as well, example PE.