Occam's Razor & PE
Tissue/cell building matrix or plastic deformation?
What’s the difference, who cares?
The difference is that the “next step” in PE knowledge can’t be taken without at least a fundamental understanding of what “happens” when we make gains.
While many here see gains as being the result of a “building” process (loosely akin to hypertrophy, of sorts) – a view which, by the way, I earlier shared – I’ve come to recognize that we are making gains by literally deforming our penile tissues.
I’ve put this theory out there a number of times, and have been soundly trashed for it, not to try to “win an argument,” but to try to motivate inquisitive members here to help us all take the next step…but we can’t seem to get beyond Step One.
I had hoped that we might see more threads regarding tissue traction and the effects of specific heat ranges for specific times on human tissue – with the hopes of optimizing our approach to PE, warm-ups, and potentially developing a minimal baseline of an effective maintenance routine/approach. Such discoveries could not only help speed up gains, but they could potentially increase gains long after the frustrating plateaus. And, of course, offer the promise of retaining those gains with the minimum hassles.
Instead, all I see are the same rehashed biological extracts (none of which relates to PE) and speculations about hypertrophy-related chemical augmentation (steroids, testosterone, etc.). Not only do I see that shit as fruitless, but it’s also a distraction from the search for knowledge of real value.
As a last-ditch attempt to stimulate inquiry into the deformation theory, I’ll lean upon Occam’s Razor as my guide. But instead of telling me that I’m “wrong,” or that you “disagree,” stop rehashing the same shit and answer 4 questions (one of which is really the $64,000 question).
If you can do so, then I’m wrong; if you can’t, then I’m right.
States that the explanation of any phenomenon should make as few assumptions as possible…. “entia non sunt multiplicanda praeter necessitatem.”
In short: “All other things being equal, the simplest solution is the best.”
This is not an exhortation to oversimplification, but rather it dismisses the Ptolemaic concept of merely “adding epicycles” when your model simply doesn’t fit the observable reality.
To paraphrase Einstein: “Theories should be as simple as possible, but no simpler.”
Simpler yet: “You can’t just keep making up shit so that your theory seems to fit.”
You cannot explain the tissue-building/cell matrix model without adding epicycles, without creating a new “quantum physics of the cock”:
(1) You must create a new quasi-hypertrophy/stress adaptation model that is unknown to medical science (indeed, that’s the very reason they reject the very theory of natural PE – because they know you cannot “buildup” the dick by exercises; unfortunately, they haven’t considered PE through the scientifically-accepted tissue traction model).
(2) You must make a quantum leap to explain why “decompensation” could require as much as 3 years after cessation of PE (as in my case) when, in all other stress-adaptation responses, decompensation occurs within a mere few weeks after the stressors have been removed (hypertrophy, suntanning, callouses, even cardiovascular fitness, etc.).
(3) You must explain not only why my losses have taken so long, but why my rate of loss has actually accelerated over time – which is the exact opposite of what occurs during true decompensation.
(4) Account for why my size losses have been greater for (consistent) flaccid than for (consistent) erect – which would also force you, necessarily, to explain why my elasticity has increased as I’ve lost size (which is the only reason why my flaccid losses could be double my erect losses).
(5) [Bonus question] Why is it so difficult, if not impossible, to achieve good gains in the glans when, ironically, the glans encounters the most stress of the entire penis from PE (especially during jelqing)?
No “Adding Epicycles” necessary with the Tissue Deformation Model
I’ve argued: PE gains are the result of tissue deformation via both externally-invoked stressors (“traction,” such as stretching) and internally-invoked stressors (“impaction,” such as jelqing, squeezes, etc.). And both forms achieve the same effects – distension of the tissues which, repeated over time, result in the deformation of those tissues.
Assumptions required? None. That view is completely in line with the scientifically-validated concept of tissue traction; albeit, applied specifically to PE.
This explains: (1) the mechanism that accounts for the size increases, (2) the reason that those size increases could remain so extraordinarily long after the stressors have been removed, and it offers insights into the unusual paradigm of losses that I’ve experienced, as well as a theory as to why glans gains are so difficult, if not impossible.
No adding of epicycles needed.
Furthermore, I’ve refined my view that: (1) gains are realized as tissue elasticity is gradually exhausted/transformed in plasticity, (2) potential gains are dictated by a guy’s native levels of penile elasticity – loosely revealed in his Flaccid-to-Erect ratio [F:E], (3) if/when size losses occur, there should be a resulting increase of elasticity (bingo!).
What the elasticity-to-plasticity (EtP) model does explain:
(1) “Decompensation” did not require 3+ years to occur; my losses had nothing to do with decompensation (since my gains had nothing to do with supercompensation). What occurred is that the (very) gradual recycling of cells in my penis finally reached a critical mass – where losses became undeniable. As my PE-deformed tissues were being “repopulated” with cells, the newer cells followed my DNA blueprint – not my PE history. In my case, this process took 3+ years to reach critical mass, and it continues.
>> I cannot stress this point enough. I did an enormous amount of PE – 5 to 7 very intense hours per week. I tracked all of my workouts with an Excel sheet, using formulas. I knew exactly how many minutes per week I stretched (not mere “clock time” but Time Under Load), I knew exactly how many jelqs I did per week – very strong jelqs, resulting in a bloated, blood-red cock. And I stretched with such force, even to the point of injury, from all angles, including dual-fulcrum stretches. Then I stopped…nothing. Cold turkey. But it took a 3-year (complete) removal of these stressors to result in decompensation response? There’s simply no model for this – which is why you must add epicycles to force the tissue growth matrix to fit.
[Note: it’s quite possible that this “return to normal” requires many “generations” of cellular recycling – else it probably would not have required 3 years to realize my losses. In other words, I’m not claiming that as soon as a “PE’d cell” dies it’s instantly replaced by a cell of your original size; but I believe this gradually does occur.]
(2) Just as newbie gains in the gym (true supercompensation) are most pronounced in the beginning of your weight training (provided that your training & dieting are proper), so is the subsequent decompensation the most rapid after the cessation of training; to be sure, your cumulative losses will mount, but they slow down, they do not accelerate. In my case, regarding PE, the opposite has occurred:
* First 18 months off PE: zero losses (apparently)
* Next 18 months off PE: 1/8” loss (both EL & EG).
[1/8” loss in 3+ years]
* Next few months off PE: 1/8” loss (measured EL only)
[equals my loss of first 3 years within only a few months]
* Past couple weeks off PE: ¼” additional loss (measured EL only)
[this doubles the loss of my first 3 years, and is double the loss also of the previous few months…3/8” loss during past few months – triple the loss of my first 3 years off PE].
Again, this is the opposite of the confirmed “tissue-growth-matrix” (hypertrophy).
[Note:  You might object that your gains were most rapid as newbie, hence doesn’t that follow the model of supercompensation? It is certainly similar, but there’s no reason why the EtP model should be any different regarding newbie gains. In both instances, training and/or PE represents a radical departure from the status quo - hence the introduction of stressors incite a profound need for the body to affect adaptation. The real difference is to be seen after the cessation of the stressors: in true decompensation, the losses are greatest (in value) at the onset of cessation. In my cases, the losses took a long time to kick in – and then they appear to be accelerating.
 You also might state that your newbie gains were nil, but took a while to kick in. This is no contradiction (in PE or weight training). All this means is that you had a higher “response threshold.” But once your gains finally did kick in, they were no doubt the most dramatic at the beginning (again, provided that you were training properly).]
(3) Gains in glans size – if they occur at all – are the most difficult to realize (as westla has corroborated in other threads). Why? Should not the “tissue growth matrix” also apply to the glans? The EtP model offers a very plausible explanation: the glans is simply too elastic. My glans inflates more (proportionately) during erection that the rest of my penis. Also, during the most severe erections – when my shaft feels like a baseball bat and I can’t seem to budge the sides with a squeeze – I can pinch my glans rather thin. As soon as I let go, my glans pops back to normal.
You simply cannot apply enough pressure (to affect deformation) to the glans without applying too much pressure to the rest of the penis. Unless you can “remove” your glans – and repeatedly hit it with an air gun – you’ll never be able to impart sufficient stressors to deform the glans…not without destroying the rest of your penis. [caution: it’s extremely dangerous to focus work just beneath the glans, because of the rich network of nerves located there; it’s always safest to focus any intense squeezing at least 1” below the bottom of the glans]
I realize that some guys claim to have made decent glans gains. If this is true, that can be explained by theorizing that their existing elasticity levels in their glans was unusually low (yet, this is a rarity indeed). If you want to see pics of a guy who basically doubled his penis size (by volume), yet apparently gained no glans size, look at my pics. In my earliest pic, my head was wider than my shaft (like a mushroom). But the end game for me, my shaft was wider (like a cucumber): big PE gains, no head gains.
Yet, if the “tissue growth matrix” were true, your glans should achieve the best gains. Why? Because during jelqing, the glans is always under the most pressure – and this pressure only increases as you complete each jelq. Yet, as your hand slides down your shaft, progressively more of your penis (between your hand and pubis) is being relieved of pressure. So, the glans gets the most work of all during jelqing, yet seems to gain the least.
(4) While my erect size has lost ½”, my flaccid size has lost a full inch. What does this mean? It means that my while my penis expands ½” less during inflation, it contracts a full inch more during deflation. To lose a full inch during flaccid (consistently), but to still come within a ½” during erection (consistently) can only mean that my penis is more elastic – else my losses, erect & flaccid, would be uniform.
This is completely inline, to the letter, with my theory that gains are realized as elasticity is gradually transformed into plasticity.
It is also consistent with my (new) belief that my “PE’d cells” are being recycled, en masse, with newer cells more consistent with my DNA. For me, this is presenting both as a loss of erect size, and a greater loss of flaccid size; hence, also a gradual restoration of my hereditary elasticity.
Am I asserting the “No” cells increase during Deformation?
No. I believe that some “bridging” occurs (possibly collagen) during the repair process. As I’ve stated, I don’t believe that we’re “creating hollows.” PE does not transform the penis into a honeycomb. But, we’re not “packing on the beef” with PE. First, the tissues must be (gradually) overstretched – deformed. Then there’s some type of repair process – but it’s not akin to hypertrophy, it merely “fills in” the damaged part of the overstretched tissue.
Based upon my accelerating losses, I’m now convinced that a 100% loss of gains is inevitable – provided that you’ve desisted from PE, cold turkey, for a long enough time.
Again, instead of dismissing this theory as “alarmist,” explain why you believe it is so.
Only, this time, refrain from conclusions masquerading as premises.
If you’re genuinely interested in advancing PE, for all of us, then keep your assumptions to a minimum…
“entia non sunt multiplicanda praeter necessitatem.”
• P.S., Whether you believe in this model or refuse to believe in this model, the reality of genetic limitations is unchanged.
One more thought: The notion of “cementing” any gain is meaningless. I am as guilty of using that word as anybody else, but if you think it through carefully…what the hell does it mean?
Would you go to a gym instructor and say, “I want to have 18-inch arms, so I figure I’ll build them to 18 ½, ensuring that I’ll ‘cement’ 18 inches – then I can quit working out,”?
Is PE “permanent”? In the relative short-term, yes. Once your tissues have been repeatedly overstretched, over a long-enough time frame, those tissues are “stretched out of shape” (therein may lie the only meaningful definition of “cementing” – and I’ve theorized that you never really “cement” your best size ever, for there’s always some retraction). But as your body recycles generations of cells, “those tissues” no longer exist.
But unlike the dynamic fluidity of hypertrophy (compensation, supercompensation, decompensation – always in flux), “cemented” PE gains could hang around for a few years.