Occam's Razor & PE

Iguana,

I want to clarify one thing and make one more point.

You know that I have a big problem with the enormously delayed onset of decompensation following the complete cessation of PE stressors (in terms of a GvM model). I hate to sound like a broken record, but that IS one of the most compelling arguments against that model…….and nobody has provided any good answers as to why the tissues of the penis would require 30-50x the amount of time typically observed in all known damage-compensation-supercompensation-decompensation paradigms.

Point to Clarify
I don’t believe that EtP applies only to connective tissue, but to the soft tissues as well.

One More Point
Ponder this: If we really are engaged in a “tissue building” process, then we’re all doing a DAMN LOUSY job. Think of the threads seeking responses from members of the “2 Inch EL Gain Club.” There are so few. After all of my enormous efforts, I have not technically gained 2.00 inches….close, but this ain’t horseshoes.

Figure, any guy starting here with a “standard” 6 x 5 (11.94 ci), shouldn’t have much trouble reaching the (curiously) much-sought-after 8 x 6 (22.92 ci).

I realize that’s a gain of 10.98 ci (a 92% increase), but still…those 2” of length should not be very tough. Yet, few guys ever attain it - even those who’ve tried manual (w/every exercise possible), hanging (from every conceivable angle) and All Day Stretchers. Some guys sleep with their wang tucked BTC all night, they wear a velcro wrap or golf weights on their dicks, sit on the dicks (fowfers) while at the computer, etc., etc.

You’d think that with 100,000 members here, if even 5% of them reached “2.00 inches,” we should have at least 5,000 guys here in the “2 inch club.” Okay, you say that 3/4 of them are newbies. Fair enough, that’s still leaves at least 1,250 guys here who should’ve topped the 2-inch EL gain mark.

But we don’t have 1,250….or 125………possibly not even 12 (and a 1/2 :) )

Maybe, I say maybe we have 8-10 members here who’ve actually hit a full 2.000 inches of EL gains (ModestoMan has said that he’s seen reasonably-verifiable evidence for only 1 or 2 such guys - out of 100,000!).

But, I’ll be generous and concede 10 (to make the math easy). 10 out of 100,000 = 0.0001. That’s only 1/100th of 1%!!!

I see this as even more evidence of exclusive EtP deformation. Let’s face it, a guy with an average F:E doesn’t have a whole lot of elasticity in his jimmy. Without much of that elasticity, there’s simply not much opportunity to enlarge a great deal.

As I’ve stated, not only am I losing size, my penis is becoming more elastic (it inflates 1/2” more than before - but since my FL is an inch shorter, my EL is still falling 1/2” short of my former EL). That only further advances the argument of EtP.

With each guy having only one dick to train (as opposed to so many muscles in the body to be hit in the gym), and with “workouts” not nearly as exhausting as gym workouts, and with such a “primal” urge or drive or desire to be hung (almost maniacal)…we should have guys here (and not just a few) that have gained 4, 5, even 6” of EL.

Think about it.

Was it this you were looking for (by Shiver), wad?

Benefits of Heat in PE

Thanks wad! I really think we are getting close to a consensus.

Ok, regarding your questions;

(1) "You spoke of smooth muscle hyperplasia, do you have any links about smooth muscle hypertrophy?"

Yes I do. I have referenced this article a few times. It is an excellent read on VSMC (vascular smooth muscle cell) growth mechanisms.
Here is an excerpt:

Notice that it states that the hypertrophy is reversible. This could be significant as far as size loss goes. I don’t know that cell numbers would ever decrease but cell size certainly could. Smooth muscle, like skeletal muscle can atrophy. See quote below.

(2)"I know that hypertrophy is an enlargement of the fibers, while hyperplasia is a dividing of the fibers - but even if we could affect hyperplasia in the penis, would not a 3-year absence from stressors still result in the shrinkage of those additional fibers?"

Absolutely! As to what happend in your case and thus likely most others, I think your first point is spot on, "Shrinkage of cell size."

I have found numerous articles that equate penile arterial insufficiency with smooth muscle atrophy. It only makes sense. We increase vessel pressure and volume through exercises. This in turn signals the body to adapt (increase tissue size and volume capacity)to compensate for the added stress. Remove the stress and the tendency is to return to the previous state. In biology this is know as homeostasis. If the penile tissues no longer have applied stressors the need for enlarged cells is removed and they shrink. I doubt the cells die. I know when a person gains weight the body produces new fat cells. When they loose weight the fat cells shrink but they are always there. This is why it is very east to put weight back on.

It is very likely that both smooth muscle and connective tissues atrophy after the stressors are removed. It’s also likely the rate and manner of atrophy is different for each. Possibly connective tissue atrophies at a much slower rate? This could explain why you lost some size rather quickly and then additional size at a later date.

On to your next post…

Still hiding stuff in quote boxes Iggy? :)

:) Yea… Hey, can I put quoted information in a different color? Is there some other way to make it stand out?

I have a hunch that CT could be the leader concerning atrophy also, while smooth muscle may just follow the elongation or atrophy of the CT.

Wad, possibly your erections provided some slight maintenance of your size during the past 3 years. It cuold be possible that your erections during sexual activity, as well as nocturnal erections slowed the rate of atrophy, but were not enough to do the work of a successful maintenance routine. So, your penis atrophied at a slower rate than if you would have had no erections at all.

Wouldn’t your erections be considered a “stressor” to some extent, even though good quality erections are not sufficient enough of a stressor to push CT into the plastic range, and therefore cause enlargement?

It seems that erections are a sufficient stressor with chemical PE, or in the case of priapism, but then the duration (length of time that the erection is maintained) of the erection is the variable that pushes the CT into the plastic range. In that case “time” makes the difference, and once again, an erection can not cause changes alone.

Could strong erections be an insufficient stressor for enlargement, yet slow down atrophy?

You could do this [ i] yada yada yada[ /i] without the extra space in between the brackets.

Your text would come out looking like this.

Can I do this?

Evidently you can. I don’t know about others, but different colored fonts annoys the shit out of me. A word or a sentence isn’t too bad, but paragraph after paragraph bothers me. Good way to get me to skip a post. :)

Hmmm… maybe I’ll just stick to quotes. :)

Wow…just glad to get this done…
wad’s Systemized EtP Theory (PDF)

It kinda sprawled. If you’re interested to read it all, hope it helps.

- wad

Wad, since you posted last here, have you any further insight?

Wad, since you posted last here, have you any further insight?

This has been dead for nine years.