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Occam's Razor & PE

Wad, fair enough. Sounds like a good framework in which to start.

Originally Posted by wadzilla
Having said that, I want to remind you about one thing – you stated that the onus was on me to prove my theory, as if the prevailing view in this forum was a “Law.” Let’s not get ahead of ourselves. Both views are theories – nothing more, at this point. So, the onus is on all of us!


Absolutely! I wasn’t just applying that statement to you. The burden of proof lies on us all. I was just saying if you throw out something new,
be prepared to back it up and defend it.

While I wait for you to summarize your information, I would like to clarify a few things and give a brief overview of my thinking on matters (I will elaborate later.)

Some things that I think should be a given in this discussion.

1. Assumptions will be made. Let’s face it, neither one of us (or anyone else who chooses to join this discussion) has a laboratory or the knowledge to conduct the proper studies if we did. When it comes down to it, we honestly do not know what goes on inside our penis that makes it larger. We can only make assumptions and conclusions based on:

a. Personal Observation
b. Observations and experiences of others
c. Studies that might relate to the same or similar tissues and/or components and
d. The outcome of testing what we assume to be true

2. We need to be reasonable. If the majority of evidence points in a reasonable direction and there is no hard core ultra specific data to prove it beyond a shadow of a doubt. It shouldn’t be just dismissed as speculation. I’m not saying it should be accepted as Gospel either. Just that it should be noted as a possibility.

This is a quote I pulled from the TGC thread and I think it says it all…

Originally Posted by 395Man
I think most everything presented in these forums, or other similar venues, mostly qualifies as “underground science”, and thus, to expect the exact same standards of quality and exhaustive study, including clinical trials, as found in the standard peer reviewed medical journals is asking for too much.


Simply said, be reasonable.

First off, understand that I don’t prescribe solely to either theory. It is my opinion that one of the biggest errors in the majority of theories around here is that they assume that ALL tissue in the penis reacts the same way to applied stress. I think the information I have reviewed over the years shows that this is simply not true. We have to remember the penis is a very complex organ with many components and facets. It is not just one big blob of tissue. Stress on connective tissue will react differently than stress on the cavernous smooth muscle within. Our approach needs to take this in mind.

So, don’t think I am dismissing plastic deformation as a valid hypotheses. I think there are components of this theory that are accurate and I have made this known in other threads/posts.

Originally Posted by Iguana
Studies show that ligaments, which are similar in composition to the tunica, are sometimes subject to plastic deformation as a result of strain. Not that cell proliferation does not occur in connective tissue; I have found articles that suggest that this does indeed occur. But the majority of articles I have read point to elastic/plastic deformation. Probably because most are in reference to connective tissue injuries. There is much less information pertaining to the growth of connective tissue as a result of mechanical stress

Iguana - An Abrupt Size Loss


But on the other hand, I don’t think plastic deformation is responsible for the enlargement of ALL tissues. Especially, the smooth muscle portion.
I think what I will present will clearly show this.

Originally Posted by wadzilla
Furthermore, the cell/growth view is actually the one that has been roundly dismissed by the medical community (in other words, their rejection of natural PE is based upon the very view in this forum regarding the “mechanism,” which the doctors know cannot happen). So, the prevailing theory here is actually the one with a big strike against it – not my theory.


Agreed. But, you also have to look at what is being purported to be the impetus to growth here; penis patches, pills, and all sorts of other “snake oil.” I think the statement “…the ‘mechanism’, which the doctors know cannot happen” is inaccurate. From my research the doctors are very aware that these “mechanisms” and processes can occur. It’s just that the advertised commercial products and processes (with a very few execptions) do not effectively invoke these mechanisms and the average Joe has no idea how or what does. Nor does any doctor in his right mind want to risk his career or reputation to research or advocate any process that does.

Originally Posted by wadzilla
The medical community has repeatedly & emphatically stated that natural PE cannot occur because the penis is not comprised of tissues that are conducive or responsive to GvM.


I don’t believe this statement to be accurate. Can GvM occur in penile tissues? Yes. Do commercial products elicit this, for the most part, no.

Originally Posted by wadzilla
I have never heard them dismiss it within the framework of EtP (I don’t doubt they would caution against attempting to deform your penis via exercises – if only out of fear of litigation – but I’ve never heard them consider natural PE within that framework).


I have actually read legitimate comments pertaining to enlargement devices from a few doctors that were not totally dismissive. Some say it is possible that some methods may work (such as traction devices) but none elaborated as to how these methods work.

Many of your comments seem to assume I am totally against the idea of plastic deformation which I am definitely not. In light of that, it would be pointless to address those comments.

I await your return… :)


Let me tell you the secret that has led me to my goal: my strength lies solely in my tenacity.

Louis Pasteur


Last edited by Iguana : 09-03-2008 at .

Originally Posted by Iguana
Wad, fair enough. Sounds like a good framework in which to start.

Absolutely! I wasn’t just applying that statement to you. The burden of proof lies on us all. I was just saying if you throw out something new,
be prepared to back it up and defend it.

While I wait for you to summarize your information, I would like to clarify a few things and give a brief overview of my thinking on matters (I will elaborate later.)

Some things that I think should be a given in this discussion.

1. Assumptions will be made. Let’s face it, neither one of us (or anyone else who chooses to join this discussion) has a laboratory or the knowledge to conduct the proper studies if we did. When it comes down to it, we honestly do not know what goes on inside our penis that makes it larger. We can only make assumptions and conclusions based on:

a. Personal Observation
b. Observations and experiences of others
c. Studies that might relate to the same or similar tissues and/or components and
d. The outcome of testing what we assume to be true

2. We need to be reasonable. If the majority of evidence points in a reasonable direction and there is no hard core ultra specific data to prove it beyond a shadow of a doubt. It shouldn’t be just dismissed as speculation. I’m not saying it should be accepted as Gospel either. Just that it should be noted as a possibility.

This is a quote I pulled from the TGC thread and I think it says it all…

Simply said, be reasonable.

First off, understand that I don’t prescribe solely to either theory. It is my opinion that one of the biggest errors in the majority of theories around here is that they assume that ALL tissue in the penis reacts the same way to applied stress. I think the information I have reviewed over the years shows that this is simply not true. We have to remember the penis is a very complex organ with many components and facets. It is not just one big blob of tissue. Stress on connective tissue will react differently than stress on the cavernous smooth muscle within. Our approach needs to take this in mind.

So, don’t think I am dismissing plastic deformation as a valid hypotheses. I think there are components of this theory that are accurate and I have made this known in other threads/posts.

But on the other hand, I don’t think plastic deformation is responsible for the enlargement of ALL tissues. Especially, the smooth muscle portion.
I think what I will present will clearly show this.

Agreed. But, you also have to look at what is being purported to be the impetus to growth here; penis patches, pills, and all sorts of other “snake oil.” I think the statement “…the ‘mechanism’, which the doctors know cannot happen” is inaccurate. From my research the doctors are very aware that these “mechanisms” and processes can occur. It’s just that the advertised commercial products and processes (with a very few execptions) do not effectively invoke these mechanisms and the average Joe has no idea how or what does. Nor does any doctor in his right mind want to risk his career or reputation to research or advocate any process that does.

I don’t believe this statement to be accurate. Can GvM occur in penile tissues? Yes. Do commercial products elicit this, for the most part, no.

I have actually read legitimate comments pertaining to enlargement devices from a few doctors that were not totally dismissive. Some say it is possible that some methods may work (such as traction devices) but none elaborated as to how these methods work.

Many of your comments seem to assume I am totally against the idea of plastic deformation which I am definitely not. In light of that, it would be pointless to address those comments.

I await your return… :)

Good post, Iguana. I just had time to pop in right now, but I hope to present more over the weekend. I don’t want to drift away from another one of my threads (I know I’ve done that a bit). I’m a single parent, I work odd shifts, my kids always have something going on.

Be back soon.

Originally Posted by Iguana

But on the other hand, I don’t think plastic deformation is responsible for the enlargement of ALL tissues. Especially, the smooth muscle portion.
I think what I will present will clearly show this.

I agree with Iguana on this issue. I doubt that the smooth muscle within the penis reacts to PE methods the same way as the connective tissue does. Yet, most all of us agree that the connective tissue is the limiting factor, aside from situations where a guy has been overworking his penis.

Now, back to the connective tissue. I want to point out that the plastic deformation theory may well include, or involve the microtear theory. This is because plastic deformation of connective tissue can also be defined where in the total length of the connective tissue has been permanently changed, or permanantly elongated. For, an example, we might say that the septum has undergone plastic deformation, yet what actually occured on the microscopic level was microfailures, or mircotears. These microscopic gaps were then filled in, or covered with more collagen (wad used a similiar example he called bridging, but he did not clarify if he believed microfailures occured first).

This is just one scenario of what may be going on in the connective tissue. I’m just tossing the idea to you guys.

Originally Posted by iamaru
… I make a point of placing a small cup of milk and plate of cookies next to my dick every night so that the PE brownies will work on my unit while I sleep.

Originally Posted by Iguana
2. We need to be reasonable.

:bart: Fine, be that way.


Running a Massive Co-Front.

Maybe I should be waiting for Wad’s in depth description of how the plastic deformation (permanent elongation) of the connective tissue is occuring. In my last reply to this thread, I mentioned the mircrotear theory… once again…. BUT, in contrast to that I would like to say that some very convincing points on this forum suggesting that we achieve permenent elongation without the formation of microtears. Pudendum has posted a thread with information to support the idea that microtears are not produced in order to permanently elongate the CT. Firegoat has also given his opinion in a broad perspective, without going into the scientific precesses. After reading posts by these two guys, as well as other post from the “thinkers” on this forum, I’m more inclined to think that permanent elongation of the CT in our penises is achieved without creating microtears. My reasons for leaning towards this belief is that scar tissue would be created, which would be very permanent (a clue that Wad’s theory may not include microtears), and secondly the CT would contract after the scar tissue formed. It may possibly even contract slightly in the following day or two. This may explain why serious cases of overworking the penis lead to a smaller contracted and sometimes sore flaccid hang.

I don’t know if my going ahead and debating the two main sides of PE theory was appropriate here on this thread before Wad commented, but I wanted to lay out some ideas and present both possible scenarios.

I used to lean towards microtear theory, but now I do not. It seems that connective tissue can be permanently elongated without reaching microfailure of the tissue. How is permanent elongation achieve then? I’m not 100% sure, but I believe that “time under tension” is the most important variable when seeking to find what will lead to permanent (OK, longterm) elongation of the connective tissues. There has been more than one scientific article pointing towards this low load, long duration stretching. “How can you explain gains from jelqing and manual stretches then”, you may say. Well, cyclic (or repetitive) loading has a similiar effect on connective tissue…. possibly… I need to research that more. Marinera posting some interesting info about cyclic loading.

Well Wad, I’m looking forward to more information from you.

I can’t say I read this whole thing that carefully, but I will respond to one part. I think that length gains, at least due to ligament stretching, are permanent. I’ve dislocated my shoulder many times, and each time it happens more easily because the ligament holding my shoulder in is stretched. It’s never going to retract to its original size… a ligament won’t do that… that’s why people (one of my friends for example) need shoulder surgery to have ligaments shortened to fix this problem.

Also, I don’t think your analogy with respect to “cementing” muscle gains is right. Of course you can’t cement a muscle gain because it needs to be exercised so it won’t atrophy. The tunica is not a muscle… it’s some other form of tissue. Take pregnant women… or really obese people… one the baby is born or a lot of weight is lost they’ll (some at least) will have permanent excess skin caused by being stretched. Maybe your theory about new cells being generated in their original size is true, I don’t know, but I think the muscle analogy is off. Anyway, whether you got the why right or not I hope shrikage over time isn’t true for everyone. I’ve had my ligament length gains for… actually now that I think about it likely over three years. Maybe girth can be more easily “cemented” by PEing continually throughout life. I would in no way want to clamp every day for the rest of my life, but maybe the gains can be kept by a simple 50 jelqs a day or something to keep things as they are.

Hey guys,

Kojack10 mentioned how he was leaning towards low-load, long duration stretches for expanding connective tissues. I am currently starting to use heat with my sessions. I’ve just finished 2 months off(during which I gained!), and gained after just one heated session(hot shower) of simply maintaining a good erection for about 30 minutes!

I was wondering Kojack10, if you knew what is meant by “low-force”? And what is meant by long duration. I was thinking that having a good erection, may satisfy this “low-force” requirement on the tunica. During this shower session, I noticed my EQ went down a bit, which may correspond to tunica expansion(it gave me an extra 0.1” MSEG).

Anyone agree with the assumption? ^

Anyone?!?

Size Loss Update

Kojack,
I want to get back soon on the reply. I have some notes scribbled, because I want to make my points more concisely. I also need to look up a few things online. But I’ve been so damn busy: work, daughter had an eye appointment, also working on a web site for a restaurant (on the side).

But I just popped in to give an update (as I promised)…

1st 3 years
EL loss: 1/8”
FL loss: seemingly none (albeit, how could really notice a 1/8” difference on flaccid, which fluctuates a lot?)

Last several months
EL loss: 7/16” (9/16” total)
FL loss: 1”+ (today, after my morning wood subsided, my unit turtled badly – probably 1 ½” less than usual, but that wouldn’t constitute a “consistent” flaccid, unless it happens consistently).

One quick response to Mick:

Regarding your analogy of the shoulder injury - that might apply if the penis were nothing but a ligament. But length increases also include: CC, CS, & tunica (not to mention other structures like the urethra).

As per the skin of pregnant women, I’ve commented on that regarding women who looked great in a bikini within about a year of giving birth. Skin also slowly retracts to normal, especially since skin cells (at least on the surface) recycle every 28 days.

Also, Mick, not only can you not “cement” a muscle, you can’t cement a suntan, you can’t cement callouses, you can’t cement CV fitness via aerobics, etc….in short, you cannot cement any stressor-induced adaptive response in the human body - including the GvM model of penile enlargement - after those stressors are removed. Indeed, the onset of “decompensation” of these “supercompensations” almost always begins within a mere few weeks…not 3+ years.

That’s not “opinion,” it’s fact.

Either my shrinkage was not due to “decompensation,” because my enlargement had nothing to do with “supercompensation,” or we’ve made a breakthrough discovery which contradicts all of the known models of the stressor-induced adaptation mechanisms.

Only my theory (EtP) doesn’t require a new “quantum physics of cock.”
And, as I’ve posted above, more losses…including greater flaccid loss…

E to P = enlargement (“gains”)
P to E = shrinkage (“losses”)


Last edited by wadzilla : 09-09-2008 at .

Ok, well all I can say is that maybe yes some skin goes back to normal, but it definitely all does not.

Also, like I said I haven’t lost any of my length gains, and it’s been more than three years.

To hell with this, I have too much on my mind. I want to get this shit out of the way, and it will take several instalments…so….

I. STRESSOR-INDUCED ADAPTION INSTANCES
(Damage-Compensation-Supercompensation-Decompensation)

(1) Hypertrophy
Damage: Fiber breakdown caused by intense anaerobic workout.
Compensation: The period of recuperation/recovery to get you “back to normal.” If you don’t believe the workout caused you to be “less,” try your max AFTER your workout. Would your missing the max just be due to fatigue? Well then, try it the very next day – when your muscles are sore as hell.
Supercompensation: Size/strength increases. It’s the body’s defense mechanism to try to ensure your survival – to be better able to protect you from all that hellish stress.
Decompensation: When you quit training, the body no longer experiences those stressors; because the body no longer “needs” that extra size/strength, it no longer retains it (gradually, of course).

(2) Suntan
Damage: Caused by UV rays – manifested by redness, even blisters.
Compensation: (The redness & blisters might be considered part of this), but the blisters resolve, the redness begins to darken…returning the skin to “normal.”
Supercompensation: Tan formation; again, a bodily defense reaction taken to avoid further burnings.
Decompensation: Tan peels, gradually fades.

(3) Callouses
Damage: Caused by friction with pressure – manifested also by redness, even blisters.
Compensation: The “healing” of the redness, blisters, getting the skin “back to normal.”
Supercompensation: The repeatedly-affected surfaces of the skin form a thick, horny callous.
Decompensation: Callouses tend to gradually flatten, smooth out, and fade away.

(4) CV Fitness (probably the most fleeting)
Damage: Caused by the extreme demands placed upon the CV system because of intense and prolonged aerobic exercise (increased heart rate, labored breathing, perspiration, increases of wastes in the blood stream, decrease of O2 efficiency, etc).
Compensation: Body rests, recovers, breathing & heart rate return to normal, wastes cycle out of the body, etc.
Supercompensation: Stronger, even slightly enlarged heart, dilation of arteries & veins, greater oxygenation/waste removal efficiency, etc., etc.
Decompensation: You lose your stamina, endurance, etc.

* - Note: CV fitness can be lost with incredible rapidity. This might not apply as much to the “casual jogger,” but I found out first-hand when I played football. Our summer “mini camp” was hellish running: 400’s, 200’s, 100’s, 40’s – all back to back to back, for a few hours. And before & after this torture were 2 laps around the track (1/2 mile before and after each session). Guys were collapsing, some were puking, etc. A mild ankle sprain caused me to miss 1 WEEK. Upon my return, despite all of the taunting by my teammates & coaches, I couldn’t even complete half of the workout. And I puked. I turned into a CV “pile o’ shit” in only 7 days.

(The onset of my PE losses required 30-50x the known time periods observed in delayed-onset losses. That’s an enormous discrepancy for which any proponent of the GvM must account – my EtP model does offer an explanation that’s more than merely “adding epicycles”.)

II. THE LOSS PARADIGM
(The nature of Decompensation)

(1) Onset
In all of these models – providing that the frequency & intensity of stressors is sufficient – the onset of decompensation occurs rather soon after the removal of the adaption-inducing stressors. And this begins within weeks – if not days – after the removal of the stressors.

(2) Manifestation
In all of these instances, the rate of decompensation is greatest soon after the onset. The initial losses will tend to be steep, with the rate of loss gradually slowing, until it evens out and eventually tapers off.

Examples –
Suntan: Decompensation can occur so rapidly that the skin actually peels & flakes off. After that initial, abrupt loss, the tan hasn’t disappeared – but it will gradually fade away (but no longer with any abrupt “losses”).

CV Fitness: Even had I continued to miss workouts, I would NOT have continued to lose at that rate – lest I ended up bed-ridden & hooked to a ventilator.

Hypertrophy: The initial losses are always the greatest, then they gradually slow until they level off.
In another thread (?) I posted about how I used to do 500-lb full-squats, and that I could still do 400 even 2+ years out of the gym. So, I lost 100 lbs over, say, 25 months. But I did NOT lose at a consistent rate of 4 lbs per month.

For example, my loss paradigm would NOT have looked like this:
1 month out: 496
2 months out: 492,
3 months out: 488, etc., etc.

Indeed, hardly! 3 months out I would’ve been lucky to hit 450-460. Yet, I would not have continued to lose at that rate (40-50 lbs per 3 months) or I would’ve soon been confined to a wheelchair.

And, on the back end, when I did 400, it’s not like I could’ve done 404 the month before. But had I waited one more month, I would’ve only been able to hit 396, etc., etc.

Initial losses steep, gradually slowing, eventually leveling off - The opposite of my PE losses.

III. THE QUALITY-QUANTITY OF STRESSORS

This is not only key to promoting gains, but it also has a direct correlation with losses.

The casual jogger (1-2 miles, 3x/week) will not turn into a “pile o’ shit” if he misses a mere week, but somebody on a tortuous regimen will. The greater the “Q-Q” of stressors, the more abrupt the losses.

Someone who just walks out in the sun to and from their car to work and home might get some sun – but they won’t burn, tan deeply or peel. But a roofer, who finally gets laid off at the end of 4 months baking on rooftops will see an abrupt decompensation.

And if a guy does intense PE for 5-7 hours per week (like I did) then suddenly stops – cold turkey – the onset of his decompensatory losses should occur within 3-6 weeks (mine didn’t begin for more than 150 weeks). His losses should be greatest in the beginning, gradually slow, before tapering off (mine was the opposite: the “baseline” was maintained for the first 150+ weeks, then gradually began to accelerate, spiking upward).

to be continued….

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