An Abrupt Size Loss

Regarding my American comments, I am myself an American (something like 8th generation). And while I know that there are very disciplined Americans, I’m also aware of the statistics: Americans make up less than 5% of the world population, but we consume something like 80% of the natural resources. We are - undoubtedly - the most overweight county on earth (by far). We need constantly catered to, we have “life coaches,” “personal trainers,” we want everything “instant,” or drive-thru (even drive-thru funerals). We are known around the world as arrogant, ignorant, fat, voracious consumers. Btw, we also have an inordinant % of the fat surgeries done around the world.

kingpole, dongalong,
I do drink quite a bit of coffee, but my intake has been pretty steady over quite a long time. Certainly no recent increases. While I’ve often wondered if a lot of caffeine is bad for PE, it didn’t hurt me during my first 3 years off.

Regarding any anxiety or dread…none that I can think of. Some of the vets here probably recall the bizarre tales & angst that assailed me as my marriage was crumbling, but that was long ago. For more than 2 1/2 years, the hellhag has been gone, I’ve had the kids and my finances are better than they’ve been in years (although, I still have a ways to go).

Those were good questions, but I just don’t think they apply much to me.

???

Links ab lout anti ageing …

Slowing down the ageing process, I watched Dr. Oz on Oprah. I only watch Oprah when Dr. Oz is on her show.

I believe that PE gains are the result of a version of “plastic deformation.” I figure that no other models could explain why I had maintained such a high percentage of my gains for such a long time after the stressors had been removed. No type of bodily stress-adaption (hypertrophy, dermal callouses, suntanning, etc.) could possibly remain for 3+ years after those reaction-provoking stressors had been removed.

Earlier, I had hastily concluded that the “changes” that were being imposed, at the cellular level, could somehow become “normative.” I believe this was inspired by reports that UV radiation could cause permanent cellular damage (which could lead to malignancy) and that some powerful substances, such as LSD, could actually result in damage/alteration to one’s very DNA (which could even subsequently increase one’s chances of having deformed babies).

As doctors have mentioned, every cell in the human body is “recycled” (within) every 7 years. These “replacement” cells don’t happen all at once, of course - nor does it take a full 7 years for every cell in the body (only that “within” 7 years, every cell is recycled).

As PE is NOT caused by radiation or powerful interactive chemicals, it doesn’t actually alter one’s DNA - it’s just a mechanical stressor. Indeed, the “deformation” of those particular cells might be irreversible, but the “blueprint” of one’s cell factory has not been altered.

I suspect that PE cannot ever be “permanent” (unless your gains resulted from a huge zap of radiation to your cock). No matter how thoroughly you deform your (present) penile cells, no matter how long you hold onto the vast majority of those gains (such as…3+ years???), once your body starts to recycle those cells, it will do so according your cellular blueprints (DNA) - not based upon your history of stretching & squeezing your cock.

Is a Total Loss Possible?
I think that might be the worse case scenario: that after all of the deformed cells of your CC, CS, ligs, connective tissues, urethra, skin, etc. has been completely recycled….you might return to the very beginning - to the cock that Nature gave you.

To guys who love to PE (I hate to PE), this probably won’t seem like too big of a deal. Nonetheless, you might be facing the prospect of life-long PE….or, you might be just a few years away from a total loss of gains.

A Possible Application of The Hypothesis
A guy starts PE, makes some gains (hopefully), eventually keeps plateauing, decides that more gains are not forthcoming, decides to do a maintenance routine. This will probably keep his losses in check - until his cells are being recycled in ever larger numbers. Once this happens, his MR will seem useless.

Growth is not because of deformation of cells, it is because there are more of them, and more matrix.

This is good! This is good!

…even chronic use of aspirin can cause ED.
…..

I also believe growth is due to creation of more cells, not plastic deformation as Wadzilla states. Good to hear others that believe the same thing!

This has been described in a stress-strain curve in 3 regions: toe, elastic and plastic region, are the tissues ability to resist elongation forces in order to prevent tissue damage. Toe region is elongation of tissue in physiological range where relatively low force is required to elongate the tissue. The elastic region represents the response of the parallel-oriented collagen fibrils to elongation, once the crimp has been removed. Elongation in this region is within its physiological capability and recovery is completely reversible. Elongation in plastic range will result in a degree of permanent tissue lengthening or if extreme, complete failure. Clinically this is the region where tissue damage occurs.

We used gene array technology to analyze differences in gene expression between mechanically stressed and relaxed fibroblasts. A number of stress-responsive genes that showed a two- to sixfold difference in their relative expression were identified. Connective tissue growth factor (CTGF) was among those genes that showed the most striking up-regulation by mechanical stress. Its regulation occurred at the transcriptional level and was reversible. A new steady state level of CTGF mRNA was reached within less than 6 h after stress relaxation. Mechanical stress was absolutely required for sustained high-level expression; TGF-β, which is also known to stimulate CTGF synthesis, was not sufficient on its own. Experiments with specific inhibitors suggested that a protein kinase and a tyrosine phosphatase were involved in the transduction of the mechanical stimulus to gene expression. Since CTGF controls the synthesis of several extracellular matrix proteins, it is likely that this growth factor is responsible for the increased synthesis of collagen I and other matrix proteins in stressed fibroblasts.

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.

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

Well. I believe both are correct. I think one thing most guys overlook is the fact that the penis in not just made up of one tissue type. The composition of the tunica and fascia is substantially different than that of the cavernous/vascular smooth muscle it encompasses. It’s only natural they would respond differently to mechanical stress.

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 infomation pertaining to the growth of connective tissue as a result of mechanical stress.

I’m inclined to belive that long term sustained stretch would be likely to produce connective tissue growth while short term intense stretch would more likely induce some type of deformation.

Connective Tissue Elastic and Plastic Deformation

Connective Tissue Growth

As for smooth muscle:

… just my two cents.