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!