The mechanisms behind PE - an attempt to give an outline that is supported by science

MoociMan

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The purpose of this thread and what we should discuss

This thread is devoted to critically discussing the theories of the mechanisms behind penilegrowth (caused by traction and PE). What we should aim at is finding some theory that, although prescientific, fits the facts and at the same time predicts, so that if it is true, it will give us a hint of the scope of the methods we deploy. It should also be refutable (if facts that seriously undermines it) comes about.

Brief discussion of some theories

I recently found another forum devoted to PE. This (and many forums like it) promote what is, in my opinion, unfounded, biased theories constructed to maximize the appealof different PE-products. I wont mention its name, so nobody should feel that I am targeting them with this criticism.

I want this discussion to be free from personal attacks. It should be devoted to critically discuss the mechanisms behind PE-caused penile enlargement. The reason I write this is because not much scientific research has been done, and the research that actually has been done muddles the boarder between what is established by the study and what is speculation.

First, let me launch an attack on the Jeztender study and how it is conjoined with speculative assumptions to give the impression that penisstretchingdevices causes cells to divide. The study conducted only establishes that each individual had grown, in average, 1.5 cm. This is taken as a confirmation of stretchingdevices being usable to extend the length and (in modest degree) the girth of the penis. This is conjoined with the thesis, that it stimulates celldivision. The latter is a thesis that is supposed to explain the growth, but it is in no way a well founded thesis. This needs to be established by specifically studying how cells respond to traction.

I am not trained in natual sciences, but I do know scientific methods, and I do know that the thesis (that traction->celldivision) is underdetermined by the empirical foundation on which it rests. It is a thesis which could explain the growth, but it is not established by the growth. It is in it self in need of further justification.

There is something that points towards the falsehood of the theory of cellular growth (I will call it C-theory or CT from here on). Many people report that, while PE is effective, they have experienced that their cocks "shrink back" after a while off of their routine. A Swedish urologist also claimed (in an article in a newspaper, so it is no scientific source, and I haven't got the article, but will try to find it) that in his opinion PE-succes was due to inflamation and/or elasticity of the flesh.

Also, some people report that stretching has made their penis thinner (2 persons on a swedish forum reported this), and 1 person reported that an increase on 1 cm after months of use of the PE-device Jes, dissappeared after not doing anything. He could maintain the gain by doing light stretching every day.

Jelging, which inflated the penis, provides a girthincrease, and for me, it seems that the increase is larger after a heavy session, then supsides and then there is residual girth which might or might not disappear. This fits the bill of some of the girthincrease being due to inflammation, yet that does not explain the girth that stays longer than 1 or 2 days.

People can enlarge their penises a lot with pumps, but here it is clear that the most extreme increase of size is due to inflammation and fluids going into the tissue (though it is in most cases harmless - even for the extreme pumpers that have conditioned their organs). Yet people report that some of the girth and lenght stays there. So there must be at least two mechanicsms in play. The first, most obvious is what we have already established. No one can claim that the tissue doesn't swell due to mainly fluids. The second mechanism would be something else.

According to the extendingdevice manifacturer, the lengthening gained by using their product is due to long term stretching stimulating cellgrowth - the C-theory. Now, one of the keywords is, according to them, that it is longlasting, lowimpact traction. So clearly, according to them, it cannot be the same mechanism that is responsible for the manual, highstress training. Is this discrimmination warranted? I mean, it seems that the increase is pretty much the same, so what basis is there to claim that manualstretching works by another mechanism than longlasting lowstress traction?

Speaking from my own perspective I have experienced a crazy spurtgrowth, and now I have hit a "plateau", it seems. I have used highstress stretching. Now, could it be that both the longlasting lowstress traction (from hereon called "LLLT") and the shortlasting highstress traction (SHT) works by the same mechanism? And could it be that this mechanism is purely mechanical (i.e. not as the C-theory claims)?

If this is the case, then we should expect that:

1) manual, highstress training is more timeefficient, yet riskier due to tearing or straining.
2) Both methods, if applied right, should yeld the same results.

I propose that the mechanism involved is really nothing but stretching the tissue. I believe that the tissue such as skin and veins can be stretched more than the collagen, but that even this can be stretched (like you can lenthen your muscles though stretching). Now, the swellingbodies are different than muscles since they are spongelike, of course with some mechanisms to restrict blood from leaving while aroused. This tissue is very elastic, and so the small cavities should be stretchable. This means that regularly forcing blood in, creating a high pressure (like jelging or clamping) could create temporally bigger cavities = bigger erections. Veins should become bulkier too, due to the internal pressure - this I have noticed on myself. The skin should become looser, perhaps permanently.

All in all, if this is the right explanaition we should expect that growth only goes to a certain extend (perhaps varying with the tissue of the person - some are more elastic than others). Most of the growth would be temporal (but could easily be maintained), and perhaps prolonged training could make increasingly more of the growth stay.

This would mean that using a tractiondevice permanently would likely only take you to a certain limit, and extending more than that would cause strians and perhaps issues with potency (burst cavities etc.). Now, this corresponds well to the prevalation of potencyproblems in the tribes that stretch their penises to freakish lenghts.

Also, my plateau which is reached after 1.8cm growth corresponds to the average growth of the study I have referenced throughout.

Anotherthing which links elasticity to the heart of penissize is peyronies disease. Due to scartissue the penis looses elasticity and becomes bend and shorter.

What do you all think? Is there anything that speaks against this? Can you supply facts that are documented that shows gains which cannot be attributed to elasticity?

I now that my views are disconcerting for those who wish to grow many inches, but at the same time we need to further our knowledge of PE to avoid injuries and also work focused. We need to understand these things to maintain gains and to maximize efficiency of our training.

Come on, add your own experiences and help enlighten us all!
 

MoociMan

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Also, this explains why warming up plays a keyrole to this whole thing.

And did I mention: I suspect that the theory advocated by the producers of tractiondevices is to give them a theoretical upperhand. If PE-succes is due to cellulargrowth, and if cellular growth is due to LLLT, then you cannot replace their product with manual excersises. Yet we see the same succes reported from manualexcersises, so if the C-theory is right, then the longlasting traction might not be key, or alternatively there are 3 mechanisms or more (swelling, elasticity and cellgrowth). I am sceptical to this, though, as the thesis seems unwarranted. Since a guy reported shrinkage, it seems that manualexcersise and LLLT cannot be distinguished, resultwise.
 

MoociMan

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I want to add that maybe the cells can be stretched out too allowing one to get passed the plateau established by the study. This is plausible, I think. But it would still mean that you need to maintain your gains with some kind of routine. Luckily it is addictive (never new addiction could be great):)
 

redbear52

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The skin has a certain degree of elasticity but contains a lot of collagenous fibers that are not very elastic. Yet, we all know that the skin has a remarkable ability to stretch to accommodate the increased volume within the abdominal cavity when women become pregnant or people gain weight.

Plastic, general, and orthopedic surgeons have used devices called "tissue expanders" to stretch both skin and fascial (collagenous) tissue progressively over time for many years. The efficacy of these devices has been well established.

Practitioners of yoga and Pilates are known to gain increased flexibility gradually and progressively over time. This comes from gradual stretching of ligaments, tendons, and joint capsules.

Physical therapists likewise are able to help patients regain full range of motion in injured joints through repeated passive and assisted active range of motion exercises targeting tendons, ligaments and joint capsules.

It is clear that collagenous tissues have some capacity to remodel and stretch in response to repeated distending forces of sufficient strength repeatedly applied. There may be some degree of cellular division going on in these remodeling processes but I believe that the process is largely mechanical in nature.

It is no great leap of faith to assume that the same response might not be manifested by the collagenous tissues of the penis, specifically the fundiform and suspensory ligaments and the tunica albuginea of the corpora when subjected to distracting forces repeatedly over time.

A lot of folks have theorized over cellular growth of smooth muscles cells or other tissue elements being a key feature of this remodeling process, but as far as I am aware there is absolutely no substantiating evidence to support it. If we could get a bunch of guys to volunteer to do PE and have their penises repeatedly biopsied over time we might answer that question, but I wouldn't hold my breath.

Many guys have experienced "newbie gains" of a certain magnitude which occur relatively quickly and "easily" after which additional gains require a much greater investment in time and intensity. I suspect that the newbie gains are the result of remodeling of those structural elements which are most susceptible to remodeling.

Fascial tissue, of which the tunica albuginea is an example, has a component of elastin fibers which are relatively easily distended. It is believed that the suspensory and fundiform ligaments are relatively more easily deformed than the tunica. And I strongly suspect that the outer 2/3 to 3/4 circumference of the tunica albuginea is more susceptible to remodeling than is the inner aspect, called the septum, where the tunica surrounding the two corpora cavernosa meet and are fused together.

I believe that once one has exhausted the "easy" gains that can be made from remodeling the ligaments and the outer circumference of the tunica, the distending forces are then taken up and resisted by the septum, which is much more resistant to remodeling, and that this becomes the new rate-limiting structure.

I also suspect that the different layers of the tunica albuginea also vary in strength and thickness from individual to individual. In some men the inner layer of tunica with its collagen fibers primarily circumferentially aligned is stronger than the outer layer, with fibers primarily longitudinally aligned. These guys will tend to gain length more easily than girth, at least at first. Later, once the initial deformability of the inner layer is exhausted, these same men may start to gain girth more easily than length, however.

Conversely, guys with a tougher outer layer of tunica will likely gain girth more easily than length, at least initially.

It may be that application of a lessor distending force over a greater length of time is as effective as application of a greater distending force over a lessor period of time. But I believe that the distending force probably has to exceed a certain threshold before it has any effect on remodeling whatsoever. Furthermore, I believe this threshold may well vary from man to man.
 
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MoociMan

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Thank you for the input!

You sound like you have some background/training in physiology? Have you read the study conducted by those italian doctors, and do you know if it was doubleblinded and how well the statistics where made?

I think it sounds like it could be true. I also believe that you are right on in what you say about the tunica, and it mirrors how (my) penis feels. I know that surgury is risky, but is it possible that some kind of weakening of the tunica and septum combined with traction could provide effective PE?

Also I don't get why no one looks into what actually happens. There are a lot of money in the market. Perhaps people are scared to find that the penis doesn't respond much to conditioning. Is it hard/expensive to biopsy the penistissue on a small group of people using some tractiondevice? Of course it would cost more than just measuring, but wouldn't it be worth putting some kind of stamp on your product? Judging from all the spammail and penissizeinterest, there must be a huge market. Unless there is nothing to find, it seems weird that nothing gets published.
 

hsarge

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The differences in tunica structure has an impact. Just one layer of tunica means greater expansion, but in many cases softer erections. Most people have two layers of tunica, one layer running lengthwise along the corpus cavernosa, the second circumferentially. An unfortunate group has three layers of tunica which is very difficult to remodel. Genetics always has the greatest impact.
 

hsarge

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Saphenous vein graft surgery to the tunica requires the cutting of the tunica longitudinally and grafting in a section of split vein tissue. This 1) weakens the tunica and 2) provides tissue that allows the tunica to expand farther as the corpus cavernosa fills with blood. This surgery is done in Italy and Egypt but has not yet been approved in the US.
 

Big Al

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Soft tissue science has already established precedents with structures similar to those found in the penis. In this forum alone you'll find references to Davis' law as well as mechanical and biological creep. I'd suggest reading Dr. Howard's latest articles [they're available on PEGym].

Besides direct tissue expansion, there's also the "passive" tissue expansion that can be had through improved blood flow.
 

bigdex

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It is my belief that PE causes fibrosis. Fibrosis and inflammation are linked. When you initially start PE the collagen fibers are weak and stretch easily. However due to repeated inflammation fibrosis occurs. Fibrosis is the laying down of tough collagen (Type I). The previously soft pliable collagen is replaced with tough collagen. The penis loses it's ability to stretch. This is what causes the plateau. If fibrosis can be prevented then it's possible that the penis will remain in it's pre-PE stretchable state. I am currently experimenting with the PAV cocktail and will report my results in 2 to 3 months. PAV = pentoxifylline, L-arginine and viagra. It is prescribed for peyronies which is essentially fibrosis of the penis.
 

Big Al

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It is my belief that PE causes fibrosis. Fibrosis and inflammation are linked. When you initially start PE the collagen fibers are weak and stretch easily. However due to repeated inflammation fibrosis occurs. Fibrosis is the laying down of tough collagen (Type I). The previously soft pliable collagen is replaced with tough collagen. The penis loses it's ability to stretch. This is what causes the plateau. If fibrosis can be prevented then it's possible that the penis will remain in it's pre-PE stretchable state. I am currently experimenting with the PAV cocktail and will report my results in 2 to 3 months. PAV = pentoxifylline, L-arginine and viagra. It is prescribed for peyronies which is essentially fibrosis of the penis.


Interesting theory, but it's not supported by facts or results- though you're definitely entitled to your "beliefs" :) Most men that train correctly note greater stretching ability and better performance over time.

You do have a point in that an injured penis may develop plaques, which can lead to Peyronie's disease.