Occam's Razor & PE

On some of the decompensations…

I notice that I do keep most of my strength when going off of weights for extended periods…

My strength is more than if I never trained. Also my muscle tone is better than if I never trained.

Also I’m not sure if I believe in microtears. More of tension on a muscle, or in the case of PE on the tunica will result in mitosis of the muscle cells. I also do belive in some Lig gains in people where the penis is bound high up.

Maxing out lig gains would result in a lowered erection angle.

“Most” of your strength still indicates decompensation. I have kept “most” of my PE gains after about 3 1/2 years from my last PE session.

Your 2nd statement appears to be a contradiction. In the 1st you say “most” (meaning less than all), in the 2nd you say “more” (which indicates a gain)….not sure how to respond.

I have stated that when I trained, in the past, I have often gained from a break - even a 2-week break. This usually indicates that you were overtraining. So, what we’re actually experiencing is “supercompensation” (from the much-needed break), not “decompensation.” However, keep avoiding the gym long enough and decompensation will surely set in.

“More of tension on a muscle, or in the case of PE on the tunica will result in mitosis of the muscle cells.”

That is an enormous assumption. How does the tunica necessarily follow the paradigm of striated skeletal muscle? In fact, those two respective tissues are extremely different from one another in all respects. What you’ve just illustrated is the underlying circuitous reasoning behind the (medically-debunked) GvM model of PE.

I also believe in some lig gains. However, I no longer believe in the eroneous assumption that “Maxing out lig gains would result in a lowered erection angle.” If you look at a cross-section, you’ll see that the suspensory ligament moves forward, from it’s rear anchor, upwards in an arching angle. It is then attached (suspended) from the roof of the “vault.” Then it slopes downward again, on it’s way to exiting the body.

Hence, lengthening the ligament does nothing to alter the “exit point.” Nor can we really stretch it enough to alter the angle of erection (this is seen in phalloplasty patients who’ve actually had the ligament severed).

I played some hooky today from work. We’ve had a steady rain all day and I haven’t felt way, so I stayed home. I’ve spent several hours on my EtP Theory…

I’ve decided to finish it as a PDF (I’m probably 60% done). I can force myself to be more concise, it’s enabled me to include some images and it will be easier to read without being punctuated by other posts - some of which alter the direction of my train of thought.

I should be uploaded the finished PDF this week, in a new thread, for ease of downloading.

wadzilla,

Your snipes are pretty good.

I will retort a small amount. On muscular gains. One who stops training will be stronger than if they had never trained, also getting back into trained shape will take a much shorter time than it took to get there in the first place.

So on the decompensation with respect to weights - you lose some but not all. “Muscle Memory” will allow you to quickly return to a much stronger state.

So there is a “decompensation” - but you don’t “lose it all” or “lose most of it”.

On smooth muscle tissues. I believe in mitosis of various portions of “flesh”, for example if you introduce “ciyllinders” into your nostrils daily - where there is smooth muscle. I believe over time by graduating to larger cyllinders that your nostrils will become enlarged.

On lig gains. I’ve looked at the charts, from different angles. It appears that the suspensitory lig if lengthened will allow the penis to leave on a straight path, as it is some arced.

That some of us have much less “inner penis” - and more “visible” penis, and some have more inner penis and less “visible” penis.

I believe thru surgery or lig gains that more “Inner penis” can be exposed.

I understand that many do not believe this, but from the information and the way I look at it, I believe it is possible.

In looking at the tunica as muscle tissues even though smooth muscle, I believe that stretching with enough force over time will allow it to become permenantly elongated.

Wad, I’m working on a few thoughts for you to ponder over but I’m still waiting on clarification of my initial question. Is it your position that enlargement is the result of deformation of ALL penile tissue types, regardless of composition and function?

Interesting thread, this.

Wadzilla, I’m looking forward to reading your pdf. I don’t know enough about the concepts discussed in order to comment, but I appreciate the efforts of those who have obviously dedicated a substantial amount of time to ruminating upon PE theory. Much better than just tugging it and hoping for the best!

Thanks again.

dj, this is totally irrelevant to what I’m saying. The point is all about decompensation - and that is an undeniable reality that occurs as a result of the removal of the adaption-inducing stressors. The only way the removal of the stressors would not cause decompensation is if the stressors did not cause supercompensation. In other words, the only reason that the cessation of training would not result in reduced size & strength is if the training did cause it in the first place.

Funny you should mention that oxymoron. I deal with it my upcoming pdf.

So, if a guy starts lifting with a 180 bench, but gets up to 435 lbs, then quits, he won’t even “lose most of it”?

Are you kidding me? That example is ME. It equals a gain of 255 lbs. “Most of it” would be, at minimum, 51% - or about 130 lbs. Do you think I can still bench 310 lbs - 12 years out of the gym?

Ergo, your claim is completely false.

Not only are you positing mitosis for PE growth (which I will disprove in my pdf), but you don’t even seem to understand the concept of cellular mitosis. Stretching those tissues (nostrils, earlobes, lips, etc.) has nothing to do with mitosis. Indeed, it’s tissue deformation - the basis of my theory, lol. And I cover this in the pdf.

The tunica is not muscle tissue. Furthermore, it’s not even the most “difficult” component of the penis - that would be Buck’s fascia.

In the pdf, I consider the possibility of a composite model. But here’s the problem - I keep getting back to the damage-compensation-supercompensation-decompensation paradigm. There are no observable instances where any type of stressor-induced GvM adaption can be maintained for so damn long (in my case, 3+ yrs) after the stressors have been completely removed.

So, let’s say it’s 80% EtP/20% GvM…then I should’ve lost 20% of my gains over that time span.
With 90% EtP/10% GvM, I should’ve lost 10% of my gains over that time.

As I kept all but 1/8” of my gains over 3+ years, perhaps 1/8” of my nearly 2” gains resulted from GvM (or, roughly 6%).

But another possibility is that there was some initial retraction after cessation of PE by tissues that had not yet been fully deformed.

gonnagetbig,
No problem man, thanks.

Wad,

It is snippets like this that cause me to devalue the rest of your posts. You say things with such certitude, but on fronts I know about you leave out quite a bite of information. I would say many times knowingly you leave it out to prove your point.

For instance, most guys that bench over 400lbs are on steroids - were you then?

Did you currently maintain your weight or weigh near as much you did then?

Gains equating to strength and size are two different things - correct?

The bench is one of the most complicated lifts a normal lifter (non-Olympic lifter) will do. Coordination can easily be 50 to 100lbs of the lift.

You may lose some muscle, but usually the ligaments usually stay. (If you were on ‘roids you will lose more of both size and strength.)

To use you as an example, I would bet if you still weigh near your old weight (higher body fat or not), within one month of training, you could bench 310lbs.

wad,

I don’t fully agree, but there is no argument. Each person is different. I lose not much more than 10% on most of my lifts with a year off, and most of it is back in under 3 months of time. Everyone is different.

On penis growth, if you want to call the penis a fascia, tissues, smooth muscle, whatever. It appears we have proven that traction methods work on these tissues as well as other tissue types.

Wad,

Nice job on the outline! Very easy to follow.

Sorry, but I’m still not clear here. Are you applying the EtP hypothesis to the entire penis or not? Your response seems to imply that you are not but you make no definitive statement one way or another.

Some thoughts on your and others’ previous posts;

Note: The following applies only to the discussion on muscle, not connective tissues.

1. While all of these body building/weight lifting references are quite interesting, they only have application in an illustrative sense.

As you are quite aware, the penis shaft contains smooth muscle not skeletal muscle. Smooth muscle behaves entirely different than
skeletal muscle and has very distinct properties. To imply the body building analogy of compensation/super-compensation/decompensation
to smooth muscle is not entirely accurate. Why? Because smooth muscle has a capability that skeletal muscle does not have…

First off, to understand what happens during loss of gains "decompensation", we must first know what happens on during gains "compensation." Agreed?
From what I am reading here, your implication is more of GvH (Growth via Hypertrophy) than GvM (Growth vs Mitosis), hence all the body building comparisons. We need to look at things from the actual anatomy of the penis. What does science and studys show as to how and why smooth muscle grows. Comparing penile growth to skeletal muscle will get us nowhere.

Skeletal muscle and smooth muscle differ substantially. One of the key differences is the growth process. Smooth muscle, like skeletal muscle, has the ability to undergo hypertrophy (the enlargement of individual cells.) But, very importantly, unlike skeletal muscle, smooth muscle has the natural ability to undergo hyperplasia (increase in cell number.) I say natural because in an adult, the mitotic properties of skeletal muscle cease. These can be (supposedly) invoked by injectable growth hormones, but do not occur under natural circumstances.

This is important…

Under your first subheading I. STRESSOR-INDUCED ADAPTION INSTANCES (Damage-Compensation-Supercompensation-Decompensation),
you list hypertrophy, suntan, callouses, and CV, fitness as examples of tissue compensation and decompensation. While these are indeed good examples of such, this list, as I’m sure you are aware, is far from comprehensive. More importantly, the list omits hyperplasia as a stressor-induced response. Before you pull out your "growth can’t occur by mitosis" gun, consider a common stressor-inducted anomaly that is widely recognized.

Angiogenesis - definition courtesy of Wikipedia

I make this point, not to say that angiogenesis is responsible for penile growth, but to show a stressor-induced hyperplasic response that defies decompensation. Let me explain.

Here you stated:

The above statement is not true in this case. Angiogensis is commonly known in two cases, cancerous tumors and cardiovascular disease. The latter is what we are interested.

John eats too much fast food and doesn’t exercise properly. As a result, his arteries become 90% - 95% blocked. While John is a walking time-bomb something interesting happens. The stress on Johns heart is immense. It is not getting enough oxygen. So, his body begins the process of angiogenesis (natural arterial bypasses.) An as a result of complex chemical and cellular changes John’s vascular system by passes the blocked arteries with new vessels and thus relieves the stress on his heart.

What’s my point? Well, 10 or 20 years down the road, John’s newly formed arteries will still be there. Even after the stress has been removed. They will not simply disappear. Here is a stressor-induced response that isn’t subject to decompensation.

Smooth Muscle Growth - copied from TCG Theory thread Iguana - Focus Your PE and Gain! TGC Theory

Enlarging the Erectile Chambers:The evidence here points to tissue regeneration (mitosis): (Growth comes from added smooth muscle tissue and cell regeneration) and hypertrophic responses (the cells themselves englarge.)

It is well documented that several factors can elicit a growth response in smooth muscle cells, including, but not limited to, stretching, injury and increased blood pressure. The following are excellent articles which support this.
http://ajpregu. physiology.org/ … ract/262/5/R895

http://physrev. physiology.org/ … t/full/81/3/999

Quote:
II. PHYSIOLOGICAL PROCESSES THAT REQUIRE VASCULAR SMOOTH MUSCLE CELL GROWTH

C. Remodeling
Vascular remodeling is a physiological response to alterations in flow, pressure, and atherosclerosis. Remodeling involves changes in VSMC growth and migration as well as alterations in vessel matrix (214). Remodeling may be classified as proposed by Mulvany based on the nature of changes in vessel diameter (inward or outward) and by changes in mass (increased = hypertrophic, decreased = atrophic, no change = eutrophic) (214). As an example "eutrophic outward" remodeling would be an increase in lumen diameter without change in amount or characteristics of the vessel such as may occur with increased flow and atherosclerosis. In contrast, "hypertrophic inward" remodeling would be defined as a decrease in lumen diameter with increased wall thickness such as may occur with increased pressure. It has been best studied in resistance vessels during hypertension. During chronic hypertension, there is an increase in vessel wall thickness hypothesized to normalize wall stress. Physical forces (wall stress and cell stretch), autocrine growth mechanisms, and paracrine growth mechanisms (EC actions on VSMC) stimulated by the hypertensive environment appear causative.

Fig. 1. Vascular remodeling. - (Sorry, can’t embed graphic)

In response to changes in blood flow, remodeling appears to be fundamentally dependent on the presence of an intact endothelium as shown by Langille and co-workers (173, 174) and by Kohler et al. (155). Because flow-induced remodeling would be expected teleologically to be mediated by changes in vessel tone and hence diameter, candidate mediators are vasoactive molecules. Among these, nitric oxide [produced by endothelial nitric oxide synthase (eNOS)] appears to play a predominant role. Recent studies show that ~70% of flow-dependent outward remodeling is due to EC nitric oxide production as determined by inhibiting production of nitric oxide with eNOS inhibitors (317). During inward remodeling in response to decreased flow, there is a coordination of increased VSMC apoptosis and decreased VSMC proliferation to effect the decrease in vessel wall mass that occurs (47). An important role for monocytes has been elucidated in remodeling, especially in response to ischemia such as occurs after occlusion of a supply artery (277). In response to increases in flow, EC express monocyte chemotactic peptide-1 (MCP-1) and monocyte adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1). The monocytes are recruited to the vessel and infiltrate and digest the media. The EC are activated by monocytes and express basic FGF (bFGF), PDGF-BB, and TGF-. These growth factors then lead to VSMC growth and vessel enlargement. In response to increased pressure, remodeling appears to be due to activation of autocrine mechanisms that stimulate VSMC growth and changes in vessel wall matrix (123, 213, 215). As discussed in greater detail in section IV, many VSMC growth factors have been implicated in the growth and remodeling of hypertensive vessels including PDGF (227, 274), TGF-, insulin-like growth factor I (IGF-I) and the IGF-I binding proteins (7), and hepatocyte growth factor (221). Paracrine mechanisms that are important in hypertension include increased production of ET-1 and angiotensin II by the endothelium.
[/quote]

http://physrev. physiology.org/ … t/full/81/3/999

Notice how increased pressure and flow stimulates an increase in mass and vessel diameter. Isn’t this exactly what we are doing with jelqing, clamping and pumping, altering the blood flow and pressure? Notice how shear stress (stress parallel to the vessel) can increase vessel diameter.

So, what’s my point in all this?

If I am indeed correct, and at least part of penile enlargement comes from smooth muscle growth, the decompensation may take on a completely different light. For instance, what happens to newly created smooth muscle cells once the stressor is removed?

I have some thoughts on this but that’s another discussion. :)

It seems that the ‘tendon/ligament model of growth’ was thrown out of the window because ‘they aren’t penis related’ and the ‘muscles growth model’ became the king, assuming that it is more related to penile tissues. It’s a big mistake, IMHO.

Also, plastic deformation, applying the Occam’ Razor, is unuseful here : elastic changes can explain what happened to Wad penis, if this is the only problem that PE knowlegde has to solve. It doesn’t means is the right answer, anyway. Occam’ Razor is a methodologic law, not a way to discover what happens in the real world.

Again, why does everyone want to keep pushing the one theory fits all approach? The penis is not a piece of gum. It’s a complex dynamic living organ with many tissue types. Why does everyone assume they all react the same way to applied stress when biological studies show they do not? Connective tissue does not enlarge the same way vascular tissue does. We need to think components not composite.

Great logical point.

I don’t know if this is directed to me, Iguana, but I’m not saying that ‘my theory fits all approach’. If you read my last post, I simply said: striatus muscle is not a good model for the penis. There isn’t (at least, not in a relevant amount) striatus muscle in the penis.

Edit: I haven’t said, also, that Wad’ theory is wrong. I said that it is so generic that I can’t understand it.