Thunder's Place

The big penis and mens' sexual health source, increasing penis size around the world.

An Abrupt Size Loss

Originally Posted by wadzilla
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.

Wad,

I would leave these Anti-American “self loathing” comments out of this section of the forum. There are plenty of places you can do that on this forum. They do not belong here.

Thanks.

Originally Posted by wadzilla
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.

???

To your original point, couldn’t stretching account for most of your size loss. I would test this theory by stretching very lightly for a a few weeks and then measure.


Last edited by SteadyGains : 08-25-2008 at .

Links ab lout anti ageing is vast and broad. Here’s one on the role of testosterone, estrogen.

Male Hormone Modulation Page 2
.. 47. Endocrine aspects of ageing in the male. 48. [Sexual .. System may change from anti- to prothr..
Http://www.lef.org/protocols/abstracts/abstr-130a.html @ 114k


Speak softly carry a big dick, I'm mean stick!

Originally Posted by kingpole

Links ab lout anti ageing …

Too much caffeine again, KP?


11 JULY 2007 - BPEL: 5.5" EG: 4.75" NBPEL: 4.5"

11 JUNE 2008 - BPEL: 6.75" EG: 5.0" Base EG: 5.5"

KingPole is my Sensei - Goal: Just a little bit more - Progress/Routine - My Pictures - Perfect Measuring Technique

The top 7 anti-ageing herbs that help lower your risk of age .The top 7 anti-ageing herbs that help lower your risk of age-related diseases - at http://thehealthierlife.com

Hope this link works it contains a list of the 7 top anti ageing herbs. So just in case it don’t work. Ginkgo and garlic top the list as well as turmeric and Korean ginseng. Shizandras and billberry.


Speak softly carry a big dick, I'm mean stick!

Regarding whether a mechanically-induced change to body tissue may be permanent: absolutely.

A few examples: ear piercing,stretched ear lobes from wearing heavy earrings, and abdominal stretch marks following pregnancy.

And, the apparent loss of 1/4” of EL over three years is small enough as to suggest nothing at all. Perhaps the first 1/8” of apparent loss was merely gains not fully cemented. And as already pointed out, this most recent 1/8” may be temporary variation, or within margin of error, so to speak.

Also, consider that, absent any PE, slight downtrends in penis size are not unusual. Thus, had you never grown by PE, you may yet have shrunk 1/4” over these past 3 years due to variables having nothing to do with a PE layoff. Attributing your apparent loss of length to a theory of inevitable complete loss of all PE gains is a bit of a stretch, yes?

Bottom line: the majority of anecdotal evidence still seems to overwhelmingly indicate the relative permanence of cemented PE gains, seems to me.


7.6 x 5.4 (goal by April 1, 2016)

Originally Posted by wadzilla
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.

Disagree. Most of connective tissue is actually extracellular matrix. Cells that make that matrix can both divide in response to stress and create more matrix, ultimately resulting in more dick. Plastic deformation has little to do with growth. Think about stretching a piece of gum or metal… when it is stretched to its new shape what does it look like? Does your dick look like it has been deformed… or does it look like a larger version of its original self?

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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).

Changes can become normative, thanks to hormones and other cellular messengers, this is why skin is different from bone, and men are different from women.

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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).

Most cells, yes.

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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.

DNA is identical in every cell in your body. Radiation and chemicals are largely powerless to create any constructive change.

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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.

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

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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.

This sounds kind of alarmist, from what you have said you lost 1/8 of an inch in three years, how long would it take to get that back, 1 week, 2 weeks? Lifelong PE for you may mean 2 weeks every 3years :violin:
Anyways, as another posters suggested the 1/8 could be from any number of factors; age, weight, diet, medications, etc.

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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.

Cells are recycled in lower numbers as we age… this is one reason why we age.


04: NBP 5.5, EG 5. 08: NBP 7 EG 5.25. Current: NBP 6.5 EG 5.25

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!


Speak softly carry a big dick, I'm mean stick!

Ginkgo can help get that 1/8” back with steady PE. Perhaps as we get older we need more PE and less decon breaks. Or shorter decon breaks. That is nothing you can gain that back rather quickly. The worse thing to do is panic! Don’t panic! Anxiety over it will shrink it more!

Besides penis size fluctuates from day to day. I have been slightly under 8”NBP for the last few days due to lasix and caffeine consumption. Hell retaining 8-10 pounds of water probably knocked off some size to. I also think the bigger the dick the bigger the fluctuations. I can get up over 6” mid shaft girth sometimes but it mostly hangs around 5.9”EG.

As long as your having rock hard erections your doing fine. Don’t be so damb about your PE habits LOL and I do mean LOL. Don’t scare me like that anymore I though you lost an inch and and 1/8th.


Speak softly carry a big dick, I'm mean stick!

Brilliant post fourofakind.

Originally Posted by kingpole
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!

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!

Originally Posted by kingpole
…even chronic use of aspirin can cause ED.
…..

Have you a link for this statement?

Originally Posted by MagnumXXL01
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!

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

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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.

http://www.physiobd.info/articles/1…nflammation.pdf

Connective Tissue Growth

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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.

As for smooth muscle:

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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/cgi/content/full/81/3/999

… just my two cents.


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

Louis Pasteur

Originally Posted by Iguana
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.

I want to chime in. I think the exact opposite of what Iguana said. It’s pretty humorist: I’m sure Iguana has read the some (or more likely far more) amount of studies that I have read on this subject; also, just to make it clear, I think he has a far more stronger scientific background than I have. So, two not uninformed people on this subject seem to have radical different point of views about :) ; this just means, in my opinion, that we really know very little on how the CT grows.

So said, I think that heavy loads, so heavy to pull above the stress-strain curve, are the cause of the new CT production; given that CT is made of cells, heavy loads gains are based on cellular growth. I think that, speaking of connective tissue, we always have to remember that we are speaking of living tissue.

Plastic deformation in an in-animated thing is a new length without new matter; plastic deformation in the case of a tendon (or ligament or tunica albuginea) is an injury : if you have a real strain to your shoulder tendon you can’t move it: it was pulled too much. When you heal from this injury, you’ll have more stuff in your tendon, as a result of inflammation and repairing; a lot of this new stuff is scar tissue, that has to maturate and has to be pulled to a longer state: if you don’t pull on the tendon to elongate it, the tendon will be shorter, not longer - despite the cellular proliferation.

If you pull with an heavy load, but slightly less then the max strain point, you’ll damage a very light amount of CT; you have a plastic deformation, without new matter, because a little amount of elastic tissue was broken; once this broken tissue will be repaired, you’ ll have a longer CT because the cellular growth, but this isn’t plastic deformation, because plastic deformation is a change in the length of a given body without augmenting the amount of physical mass in that body.

In the last, the true plastic deformation can happens with low, prolonged loads. You’ll have creeps in the tissue, but at a so slow rate that in the body there is never a real injury nor a micro-injury : so, the CT isn’t broken, so there isn’t an high total amount of cellular growth (nor in number, neither in size). The tissue just looses it’s elasticity, and get adapted to a new, longer shape.

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