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Thoughts on PE from johndough

Creep and plastic deformation of the Tunica Albuginea
I’m still going to read more about stretching and reconfiguration of the fiber matrix within the tunica albuginea even though I am 99% sure it is a dead end. I feel it is because the rare cases where the tunica albuginea was permanently stretched and erectile function was not destroyed the reports still indicate a decreased erection quality through decreased elasticity. The elastic feature of the inner columns of the tunica albuginea is what actually causes a stiff erection. If these structures are compromised by plastic deformation, then the erection will not function as it originally did. This means that if your penis can still obtain erections after some form force stretching it beyond capacity: priapism, excessive pump or stretching then it will never be as hard as it was initially because those internal structures have been altered so they no longer function as intended. They lost their elasticity, meaning the compressive force they would exert when stretched is now diminished and would be diminished relative to the amount it was stretched beyond initial capacity.
It will be argued that slow gradual changes in the tissue through creep is the mechanism through which PE is possible. I rebuttal that in the case of ligaments this is possible, but the increase in ligament length has not been shown in the literature to improve erectile length, only flaccid length. This was determined through post examinations and studies tracking lengthening phalloplasty (ligament cut followed by weights). In the case of the tunica albuginea I have not seen enough evidence regarding the remodeling of the fiber matrix to indicate that its elastic properties would be maintained. I highly doubt they would from what I have read so far even gradual stretching of ligaments (creep) will permanently deform them and cause a loss in their elastic properties. As for studies that counter the creep hypothesis in tunica albuginea: the two pumping studies showed no difference in girth and only the second study showed a difference in length which is attributed to the reduction in Peyronie’s curvature. Pumps and regular use of vasodilators are the best argument for creep for the tunica albuginea, stretching is confounded by ligaments being stretched, yet no studies that have been conducted noticed significant changes in penis size using pumps or vasodilators.
Saphenous vein grating does support creep for increasing penis size, but not in the tunica albuginea. A study found regular use of a pump following a saphenous graft applied to the tunica albuginea lead to greater increase in erect diameter. It was hypothesized that the veinous tissue stretched under pressure of the increased blood from the pump. A second study indicated a far higher rate of erectile dysfunction in the graft procedure, as high as 13% for one of the techniques (I believe their are two techniques: 1 for length, 1 for girth), and other complications such as decreases erection quality. So, creep with maintained function is possible in veinous tissue, but we already knew this from leg extension procedures. The issue is whether the tunica albuginea can maintain function after experiencing creep, the evidence so far does not support that conjecture.

I will finish reading the links Marinera sent me and will respond to the studies and ideas listed within those links.
Keep sending me stuff and I will go through it in my spare time.

Originally Posted by johndough123
Creep and plastic deformation of the Tunica Albuginea
I’m still going to read more about stretching and reconfiguration of the fiber matrix within the tunica albuginea even though I am 99% sure it is a dead end. I feel it is because the rare cases where the tunica albuginea was permanently stretched and erectile function was not destroyed the reports still indicate a decreased erection quality through decreased elasticity. The elastic feature of the inner columns of the tunica albuginea is what actually causes a stiff erection. If these structures are compromised by plastic deformation, then the erection will not function as it originally did. This means that if your penis can still obtain erections after some form force stretching it beyond capacity: priapism, excessive pump or stretching then it will never be as hard as it was initially because those internal structures have been altered so they no longer function as intended. They lost their elasticity, meaning the compressive force they would exert when stretched is now diminished and would be diminished relative to the amount it was stretched beyond initial capacity.
It will be argued that slow gradual changes in the tissue through creep is the mechanism through which PE is possible. I rebuttal that in the case of ligaments this is possible, but the increase in ligament length has not been shown in the literature to improve erectile length, only flaccid length. This was determined through post examinations and studies tracking lengthening phalloplasty (ligament cut followed by weights). In the case of the tunica albuginea I have not seen enough evidence regarding the remodeling of the fiber matrix to indicate that its elastic properties would be maintained. I highly doubt they would from what I have read so far even gradual stretching of ligaments (creep) will permanently deform them and cause a loss in their elastic properties. As for studies that counter the creep hypothesis in tunica albuginea: the two pumping studies showed no difference in girth and only the second study showed a difference in length which is attributed to the reduction in Peyronie’s curvature. Pumps and regular use of vasodilators are the best argument for creep for the tunica albuginea, stretching is confounded by ligaments being stretched, yet no studies that have been conducted noticed significant changes in penis size using pumps or vasodilators.
Saphenous vein grating does support creep for increasing penis size, but not in the tunica albuginea. A study found regular use of a pump following a saphenous graft applied to the tunica albuginea lead to greater increase in erect diameter. It was hypothesized that the veinous tissue stretched under pressure of the increased blood from the pump. A second study indicated a far higher rate of erectile dysfunction in the graft procedure, as high as 13% for one of the techniques (I believe their are two techniques: 1 for length, 1 for girth), and other complications such as decreases erection quality. So, creep with maintained function is possible in veinous tissue, but we already knew this from leg extension procedures. The issue is whether the tunica albuginea can maintain function after experiencing creep, the evidence so far does not support that conjecture.

I will finish reading the links Marinera sent me and will respond to the studies and ideas listed within those links.
Keep sending me stuff and I will go through it in my spare time.

If a normal penis is about 50% smooth muscle, don’t you think analysing the stretching mechanism on smooth muscle type cells could provide some useful insights ?

Mechanical Stretch Simulates Proliferation of Venous Smooth Muscle Cells Through Activation of the Insulin-Like Growth Factor-1 Receptor
http://atvb.aha journals.org/cg … short/27/8/1744

Mechanical stretch stimulates growth of vascular smooth muscle cells via epidermal growth factor receptor
Mechanical stretch stimulates growth of vascular smooth muscle cells via epidermal growth factor receptor - PubMed


Starting stats: 6.4" / 5.6" Current Stats: 7.4" / 5.8" Short term goal: 7" / 6" Long term goal: 8" / 6.5"

According to the aerodynamic models known to man, bumble bees cannot fly. But we all know that they can, therefore the knowledge of mankind is incomplete.

This may help you to understand PE.

Originally Posted by stuzilla
According to the aerodynamic models known to man, bumble bees cannot fly. But we all know that they can, therefore the knowledge of mankind is incomplete.

Well, it was a nice try - but more modern studies of aerodynamics have proven the earlier studies wrong. Search: “Dynamic Stall”

I don’t think anyone is saying that priapism or sickle cell anemia are good things. Certainly there have been cases of priapism and megalophallus associated with sickle cell that have resulted in permanent impairment of erectile function. But it is clear evidence that the tunica albuginea can remodel and enlarge in response to stress.

Nor is it clear that ED resulting from priapism is due to a change in structure of the tunica or a loss of elasticity. It may very well be a result of prolonged tissue hypoxia.

Loss of elasticity is often used to describe a condition in which the number of elastic fibers in the tunica is decreased and the elastin component is replaced with collagen fibers. This does not necessarily imply that erectile function will be impaired. It is conceivable that plastic deformation of the tunica (if it occurs) could result in impaired erectile function is some individuals, but I know of no reason to assume a priori that it would always, or even usually do so. In fact, I think it is “loss of elasticity” that is the reason that many guys who do PE notice a significant increase in flaccid size, which most do not perceive as a negative.

Whether pumping ever results in permanent size increases or not is a matter of debate. There are long-term pumpers who feel that it does, especially when coupled with other forms of PE, but there are others who do not. Even those who do feel that it results in permanent gains indicate it is far more effective in increasing girth. There is absolutely no reason to conclude that pumping would be the most effective way to elongate the tunica albuginea.

Furthermore, in science “absence of proof” is never “proof of absence”. To say that one small study with a poor pumping enlargement protocol, and poor statistical power, that showed a length increase that failed to reach statistical significance “proves” that all forms of PE are ineffective in achieving remodeling of the tunica albuginea (so as to increase length) is absurd, in my opinion.

Until recently, according to the aerodynamic models known to man, bumble bees could not fly. However it was obvious that they could. It was the discovery of the Dynamic Stall that improved the knowledge of mankind.

It may help you to understand PE, if you conceptualise that the Dynamic Stall of the penis is yet to be discovered.

;)

Originally Posted by stuzilla
Until recently, according to the aerodynamic models known to man, bumble bees could not fly. However it was obvious that they could. It was the discovery of the Dynamic Stall that improved the knowledge of mankind.

It may help you to understand PE, if you conceptualise that the Dynamic Stall of the penis is yet to be discovered.

;)

Actually, the story was never true, it started out as a joke from a drunk engineer

http://www.stra ightdope.com/co … mblebees-to-fly

We knew bumble bees could fly even before we knew about delta wings

[Blockquote]According to an account at https://www.iop … cs/News/0012i.1 , the story was initially circulated in German technical universities in the 1930s. Supposedly during dinner a biologist asked an aerodynamics expert about insect flight. The aerodynamicist did a few calculations and found that, according to the accepted theory of the day, bumblebees didn’t generate enough lift to fly. The biologist, delighted to have a chance to show up those arrogant SOBs in the hard sciences, promptly spread the story far and wide.

Once he sobered up, however, the aerodynamicist surely realized what the problem was—a faulty analogy between bees and conventional fixed-wing aircraft. [/blockquote]

But the story was fun to re-tell and thus there are people who believed engineers once thought bees couldn’t fly when in fact they never thought that, just one drunk guy for a very short while and nobody else

This entire thread has been fun and educational

I had begun to speculate that most gains claimed by pe’ers was initial, myself included, I gained one inch right off the bat

However I explained that to myself by using a muscle analogy, whence most parts of our body are not extended to their maximum potential but with a little work we can reach that potential, gains after that become far more difficult

So I see on this board just about everyone gained about 1” over time, I think those with larger phallus have a greater gain potential simply due to percentages.

I read tons of bathmate threads, everone’s enjoying the device but nobody can make an actual claim for permanent growth

In addition, all of these devices that do make claims seem to make those claims based on an initial measuring, I don’t see any comparisons with someone who has already pe’d.

In the end I believe anyone who has not pe’d can gain an inch or so, give or take depending on the state individual state of relative maximum potential

If there are gains to be had after that they are certainly harder to come by and might indeed be at the sacrifice of eq or penile stability

I do however believe there is potential in severing the ligament, extending a portion of the inner penis and then re-attaching that ligament to an ideal location for erect angle and stability

Never the less, I will continue my pe excersizes, I like them and if there is potential I want it

Although the analogy can stand, what is strange is that people who starts smaller tend to gain proportionately more. So, this 1” limit could just be due to satisfcation with that for most of members.

It is true anyway that after the 1x0.5 mark gains become really hard.

Originally Posted by p6inch
Actually, the story was never true, it started out as a joke from a drunk engineer

http://www.stra ightdope.com/co … mblebees-to-fly

We knew bumble bees could fly even before we knew about delta wings

[Blockquote]According to an account at https://www.iop … cs/News/0012i.1 , the story was initially circulated in German technical universities in the 1930s. Supposedly during dinner a biologist asked an aerodynamics expert about insect flight. The aerodynamicist did a few calculations and found that, according to the accepted theory of the day, bumblebees didn’t generate enough lift to fly. The biologist, delighted to have a chance to show up those arrogant SOBs in the hard sciences, promptly spread the story far and wide.

Once he sobered up, however, the aerodynamicist surely realized what the problem was—a faulty analogy between bees and conventional fixed-wing aircraft. [/blockquote]

But the story was fun to re-tell and thus there are people who believed engineers once thought bees couldn’t fly when in fact they never thought that, just one drunk guy for a very short while and nobody else


Oh well, back to the drawing board … flying pigs anyone.

Originally Posted by alin
If a normal penis is about 50% smooth muscle, don’t you think analysing the stretching mechanism on smooth muscle type cells could provide some useful insights ?

Mechanical Stretch Simulates Proliferation of Venous Smooth Muscle Cells Through Activation of the Insulin-Like Growth Factor-1 Receptor
http://atvb.aha journals.org/cg … short/27/8/1744

Mechanical stretch stimulates growth of vascular smooth muscle cells via epidermal growth factor receptor
Mechanical stretch stimulates growth of vascular smooth muscle cells via epidermal growth factor receptor - PubMed

Thanks Alin, I will read tese later when I have a little more time.

Originally Posted by redbear52
I don’t think anyone is saying that priapism or sickle cell anemia are good things. Certainly there have been cases of priapism and megalophallus associated with sickle cell that have resulted in permanent impairment of erectile function. But it is clear evidence that the tunica albuginea can remodel and enlarge in response to stress.

Nor is it clear that ED resulting from priapism is due to a change in structure of the tunica or a loss of elasticity. It may very well be a result of prolonged tissue hypoxia.

Loss of elasticity is often used to describe a condition in which the number of elastic fibers in the tunica is decreased and the elastin component is replaced with collagen fibers. This does not necessarily imply that erectile function will be impaired. It is conceivable that plastic deformation of the tunica (if it occurs) could result in impaired erectile function is some individuals, but I know of no reason to assume a priori that it would always, or even usually do so. In fact, I think it is “loss of elasticity” that is the reason that many guys who do PE notice a significant increase in flaccid size, which most do not perceive as a negative.

Whether pumping ever results in permanent size increases or not is a matter of debate. There are long-term pumpers who feel that it does, especially when coupled with other forms of PE, but there are others who do not. Even those who do feel that it results in permanent gains indicate it is far more effective in increasing girth. There is absolutely no reason to conclude that pumping would be the most effective way to elongate the tunica albuginea.

Furthermore, in science “absence of proof” is never “proof of absence”. To say that one small study with a poor pumping enlargement protocol, and poor statistical power, that showed a length increase that failed to reach statistical significance “proves” that all forms of PE are ineffective in achieving remodeling of the tunica albuginea (so as to increase length) is absurd, in my opinion.

I think you are correct in stating that the tunica can be permanently deformed, but I do think the function will be impaired in those cases relative to the amount of deformation that took place. The loss of elasticity hypothesis is not mine, it was developed by the researchers investigating megalophallus as a sequela of priapism. The hypothesis fits the evidence I have reviewed. In regards to your point about the resulting ED possibly being due to hypoxia, I would say that hypoxia can certainly damage tissue, but would offer the following analogy to demonstrate the damage is not solely due to oxygen deprivation. If someone pumps up to a very high pressure and only holds it for a few minutes their resulting damage will not be due to hypoxia because the blood oxygen levels in the CC will still be high. Therefore, in a similar situation to a rapid onset of priapism, but without the hypoxic environment tissue damage would still occur. I agree with you that permanent increase in flaccid size could very well be due to loss of elasticity as elastin fibers have either lost their retractile ability or have diminished in number from long term stretching. However, I do not see how a loss in elasticity would be beneficial for an erection.

As for the studies, its more than just one study that counters the hypothesis that plastic deformation of the tunica could lead to penis enlargement while maintaining full erectile ability. Although, most studies did not test this directly they provide us information about how collagenous tissues respond to stress and plastic deformation. Its not all just theory either, there are two pump studies that tested pumps and measured enlargement as a parameter. Neither found anything significant in regards to enlargement. I understand the sample sizes were small, but I don’t think you can state that there would have been an effect if the power was higher until we look at the p-value. The p-value will reveal whether a possible hidden effect was there depending how close it was to being significant, if it wasn’t close then there was no effect because n>30 and the sample size was sufficient to be representative of the population. Neither of us can further debate this point until we get a hold of the p-value from the full article of the study. Your point about girth is well taken, I would expect pumps to provide more expansion in girth than length as that is what the anecdotal reports indicate. However, girth was measured too in the pump studies and no change was detected. Its not just an absence of proof, its studies that actually counter the claim. I am not just saying manual penis enlargement probably doesn’t work because there is no evidence to support it, I’m saying it probably doesn’t work because there is evidence to show it does not work both in practice (pump studies)/post surgery reviews (hanging), and in biological theory. We have anecdotal evidence, that is enough for me to say it is worth investigating further, but not enough for me to believe it.


Last edited by johndough123 : 01-15-2011 at .

Originally Posted by matutinal_euphony
I love how all the newbies explain the facts. Who cares what a urologist says? They are not experts in natural PE. People here are practically recycling the same old idea that PE does not work. I hate to break the news but it certainly does work.. :-) Can the tunica be stretched? Damn right it can, try an ADS and let that prove it for you. Can the ligaments be stretched? Damn right they can. Don’t expect the medical literature to help you much with PE. Listen to the big gainers here- they are the experts over any PhD you’ll find.

All I had to read was post number 4 right here. These so called “experts” have no idea what is achievable. The penis doesn’t just stretch, it rebuilds. It’s like working out. Muscles grow bigger as the micro-tears caused by exercising are healed and it is the same with penile tissue.

Originally Posted by johndough123
Its not all just theory either, there are two pump studies that tested pumps and measured enlargement as a parameter. Neither found anything significant in regards to enlargement. I understand the sample sizes were small, but I don’t think you can state that there would have been an effect if the power was higher until we look at the p-value. The p-value will reveal whether a possible hidden effect was there depending how close it was to being significant, if it wasn’t close then there was no effect because n>30 and the sample size was sufficient to be representative of the population.

I’m not sure if this is the pump study you guys are referring to but p values are given? But even if it isn’t the one, we had posted the abstract previously and here’s the full study and the protocol used. Maybe you guys can look through it and comment.

“The role of vacuum pump therapy to mechanically straighten the penis in Peyronie’s disease.”


Starting Size: April, 28, 2010: NBPEL-7" Girth-6" (base, MSG, glans)

Currently: BPEL-8" NBPEL-7.25" Girth-6.25" (base)/6.125" (MSG)/6.125" (glans)

Thanks, Bohm. This is one of the two pump studies, I have access to this one. We need the p-value from the other study. This study did find an increase in length, but the researchers state that it fits with the correction in angle of curvature as the patients had Peyronie’s. They don’t give the p-value for the girth in this study, but they state they saw no increases. The other pump study lasted 6 months and its primary objective was to measure size gains from pumping in individuals without Peyronie’s disease. If length gains would have been detected in this study they would not be attributable to curvature correction and would be a real PE gain. The study found no significant difference for length or girth. This is the study Redbear and I were referring to that we need the p-value to determine if there was a possible hidden effect.

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