Yet another theory of how we grow

I’m referring to “Textbook of Medical Physiology” by Arthr G. guyton; it says that cells regeneratione is regulated in so way that number and dimension of cells is relatively constant in the body. If a tissue of the body becomes bigger this is caused by:

1) hyperplasia :no proof that this phenomenon happens in the human body;
2) hypertrophy : this is quite a normal way to adapt to a stress (like atrophy, inverse phenomen);
3) cellular proliferation, a consequence of :
a) mechanical separation in some tissue (in example a skin-cut, or liver separation) - but yo’ll have scar tissue, in a certain degree and at least temporarely;
b) Cancer.

It seems that only hypertrophy can be involved in PE; we don’t cut our penis hoping it will be addictional tissue by new born cells, and don’t hope to provoke e penile cancer. Neither bodybuilders cut their muscles hoping the’ll start to grow trough cells proliferation.

Let’s define scar. Dorland’s Medical Dictionary:

“…a mark remaining after the healing of a wound or other morbid process…”

This process is via replacement existing cells. With the exception of the nerve cells in the brain or heart muscle cells (at least as far as we understand today, with a few recent reports showing this may not be correct either), almost every other tissue of the body has the capacity to repair itself with new cells (of like kind) in response to injury. Scarring, for the most part, does not infer replacement of cells by ones other than normally populate the region. There is generally a hyperplasia of normal cells in the affected tissue (by stimulation of local growth factors and not as a general rule hGH). There may be an overgrowth initially, but for the most part the repair is complete when the appropriate structural conformation, integrity and strength are achieved. This may involve subsequent cell reduction.

Proof is lacking for or against. My hypothesis is that PE induces tissue damage that is repaired by replacement of dead cells or repair of existing injured cells by the same processes that are involved with injury repair in other tissues. I’m still not sure what your hypothesis is.

A hypothesis is “…a supposition that appears to explain a group of phenomena and is assumed as a basis of reasoning and experimentation” (Dorland’s Medical Dictionary). Neither of us have found evidence in the medical literature regarding the repair of the penis resulting from PE injury (because it doesn’t exist) to confirm or deny our hypotheses. In addition, neither of us have designed or performed a studies to gather evidence to prove or disprove our hypothesis. And we have not funded or can we afford to fund (even if we could get researchers to buy into our scientific curiosities) any research of this kind. So all we can do is infer from other like tissues (for example connective tissue repair).

There is a wealth of evidence regarding tissue repair. It would seem unusual to me to consider that the penises response to injury would be any different then any other tissue. I like my penis and think “he’s” important, but it would be arrogant of me to think that it is better than any other part of my body and therefore has a different response to injury.

You use the word biochemical with regard to enlargement. I do not know what you mean.

Biochemical processes are a series of chemical reactions that take place within a cell that are catalyzed by enzymes. PE apparently affects through cell injury and cell repair or regeneration. Do you mean that since the cells that remove the dead cell debris or the growing new cells must crank up their metabolism that this mean that the enlargement process is a biochemical one and not a cellular one? I believe we’re talking semantics here.

I met and talked with Art at a number of scientific meetings in the early 1980’s. Sharp mind. Too bad he had to spend much of his life on crutches. The most amazing thing is he wrote that book and all of the subsequent editions (until he died) by himself.

I’m with you there.

This statement is absolutely positively, incorrect.

Hyperplasia is defined as “…the abnormal multiplication or increase in the number of normal cells in normal arrangement in a tissue” (Dorland’s Medical Dictionary).

Benign Prostatic Hyperplasia (BPH; enlarged prostate with age) is an example of the abnormal multiplication of the structural component (stroma) versus the fluid producing portion (glandular) of the prostate.

Normal tissue repair of an injury through cellular regeneration is an example of the “increase in the number of normal cells in normal arrangement in a tissue.”

I agree.

In my opinion this infers the replacement of dead tissues with other cells that have a different function. For example the replacement of dead nerve cells in the brain by glial cells or astrocytes; or the replacement of dead heart muscle after a heart attack by nonfunctional fibrous tissue.

My opinion regarding scar ring is stated in the previous post.

How can you make this statement? This is your hypothesis (I explain this in the previous post as well). The evidence of repair in other tissues does not support you. If you can gather evidence to support your hypothesis, I’m listening.

What I said is that there is a limit to the degree of regeneration after injury. PE does not induce injury (hopefully) severe enough to negate the process of cellular regeneration (hyperplasia).

I have read again my last post; it seem clear to me, however: my medical textbooks say hyperplasia is not observed in (human) connective tissue except in case of ablation (mutilation), cancer, and other patologic cases. If you are saying these books are wrong, it’s your burden to report some reference about hyperplasia in safe human’ connective tissues.

Even your Dorland’s definition validate what is written in that books:”…the abnormal multiplication or increase in the number of normal cells in normal arrangement in a tissue” : what does means abnormal here?

I want to add a Wikipedia extract:

…………..
<<In addition, animal tests have shown that stretching a muscle can trigger hyperplasia though this phenomenon has yet to be confirmed in humans.[2]>>
…………………….

Some of the more commonly-known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:

Congenital adrenal hyperplasia

Endometrial hyperplasia - Hyperproliferation of the endometrium, usually in response to unopposed estrogen stimulation in the setting of polycystic ovary syndrome or exogenous administration of hormones. Atypical endometrial hyperplasia may represent an early neoplastic process which can lead to endometrial adenocarcinoma

Benign prostatic hyperplasia also known as prostate enlargement.

Hyperplasia of the breast - ‘Hyperplastic’ lesions of the breast include usual ductal hyperplasia, a focal expansion of the number of cells in a terminal breast duct, and atypical ductal hyperplasia, in which a more abnormal pattern of growth is seen, and which is associated with an increased risk of developing breast cancer. The biology of these lesions is the subject of dispute, with some authorities arguing that both of these lesions are the result of neoplasia, and that the application of the term ‘hyperplasia’ in this instance is “inaccurate”.[3]

Focal epithelial hyperplasia (also known as Heck’s disease) - This is a wart-like growth in the mucous tissues of the mouth or, rarely, throat that is caused by certain sub-types of the human papillomavirus (HPV). Heck’s disease has not been known to cause cancer.

Sebaceous hyperplasia - In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.

Compensatory liver hyperplasia - The liver undergoes cellular division after acute injury, resulting in new cells that restore liver function back to baseline. Approximately 75% of the liver can be acutely damaged or resected with seemingly full regeneration through hepatocyte division, ie hyperplasia. This is the basis for living-donor liver transplants.
…………..>>

So said, hyperplasia is not the “default” way to restore or enhance human’ connective tissue’s functonality/volume, and likelyhood is not the mechanism on while PE-gains are produced.

Hope it’s clear.

MM,

I would have to go back and check my records, but from memory I gained about 1/2 inch in my first couple of weeks.

While I wouldnt call it instantaneous, it certainly was very, very quick.

At the moment I think plastic deformation (PD) is happening in PE, but I’m not sure it’s as easy as one might think.
(A Possible Breakthrough. About TIME !, Microtears Result in Plastic Deformation)

It’s true PD should make a gain permanent instantly - when it happens! However actually reaching PD is the whole challenge, in my opinion, and that can take time and a lot of effort. But thinking you’ll reach PD instantly, without injury, is not correct unless perhaps you are a lucky newbie with very unconditioned tissues. It is something you have to build up to - accumulation!

There’s a certain range between your current BPFSL and the BPFSL you need to reach before PD happens. Just because someone stretches beyond their current BPFSL doesn’t mean they reach PD, you have to stretch a certain amount beyond your BPFSL to reach it (some claim 3-5%). There’s a threshold, if you don’t reach it and stop PE your tissues is going to go back to normal. You need to keep accumulating strain/creep until you reach the point of PD. The good news is you don’t have to do all this in one session.

Every time we stretch the tissues we generate some creep/strain that last for a certain amount of time (some say 10 x the stretch time). This creep/strain we’ve accumulated in one session will slowly go back to normal, so the key is to stretch again before it has gone back to it’s normal size. By doing this we are accumulating creep/strain. This means that we can accumulate creep/strain for days, weeks or months and sooner or later we’ll reach the point of PD and the gains become permanent.

As you can see I don’t think gradual gains disproves the PD theory.

Just my 2 cents.

I wish that was my body!

Not to be overcritical: I think there is more than a grain of truth in this model; but, from a logical point, it make no sense. Let’s define current BPFSL: this is the max length of the penis when streched, taking the measurement while pushing the ruler against your pubic bone.

Now: how you can go beyond your BPFSL? If you can get a measurement of, for say, 20 cm today, when your recorded BPFSL was 19.5 cm, than your current BPFSL isn’t, today, 19.5 cm but 20 cm.

This make even less sense: let’s suppose you aren’t able, the day 1 of PE work, to go beyond 19 cm (current BPFSL), nor the day 2, neither the day 3; then, the day 4, you are able to get 19.5 cm (BPFSL *(1.03)); you are saying that now PD starts and gains become permanent. But we could say: you are looking at gains already here and you are calling it PD, whereas this is not the cause, but the effect.

I think PD could have some sense, for us, as regarded of lossen of elasticity of tunica.If the tunica is stretched for a given amount of time below it’s previous experienced length (or girth), it (the tunica I mean) start loosing elasticity. Since a given degree of elasticity of tunica should be a sort of a constant, the body start lengthening and thickening the tunica, so it could be both more able to extend over a given length (girth) and more resistant to pressure/tension.

This could explain why many achieve length and girth with lenght PE-work alone.

This should means, also, that trying to go beyond actual BPFSL is not a must (and I think could be dangerous); what really counts is that the penis is, for a given amount of time, in a longer/fatter state than normal.
That’s why extenders’ manifacturers suggest starting to use these devices with a length slightly higher than FL (not SFL, neither BPFSL); they suggest, actually, that too much tension is counter-productive. I’ve never read of good long-term gains by those who tried the “force to beyond the BPFSL” approach with extenders; those who gained with extenders where using really ligth tensions.

I don’t know if anyone has mentioned it, but I believe sleep is a factor as well. Everything recovers while you sleep. If you don’t get enough sleep, you don’t get full recovery.

Hi marinera

The threads I linked to goes into these concepts I’m trying to explain in detail.

But let’s play with some numbers. A BPFSL is 18 cm and we assume PD occurs at 3% strain meaning when the penis is 3% longer than it’s current length PD occurs and the increase in length become permanent (I’ll use length gains in this example).

So an increase of 0.54 cm is needed (3% of 18 cm) for PD to kick in in this case. In other words you need to reach 18.54 cm BPFSL. Here’s the kicker, even if you reach 18.4 cm or anything less than 18.54 the increases are not permanent and will slowly diminish if you do not maintain them and/or keep accumulating strain. Proper frequency is the key, without it you might be going one step forward and one step backward over and over again and wasting time. It’s very important to add new strain before the previous strain has fully recovered.

I think it’s a gradual process where you keep increasing the length little by little, day by day until you finally enter the plastic range. I also agree that too much tension is bad, I use low to medium tension, just enough to stretch it out 100% and then just a little more. Your point about the extenders is a good one because I can’t see how PD would explain gains from only stretching the penis slightly longer than the FL.

This is just a theory, I’m not saying it’s fact, it’s just that I think that PD is involved in PE. Maybe it’s wrong, who knows. That’s not to say other important things do not happen as well.

Dicko7x5: I think you’re referring to visco-elastic creep, which I regard as a different phenomenon from plastic deformation. Creep happens over time, whereas PD happens almost instantaneously.

I know that physical therapists have been able to elongate ligaments using repeated applications of stress (static progressive stretch or dynamic splinting). The visco-elastic creep that follows the application of stress to ligaments is said to “accumulate,” causing permanent elongation of the ligament.

I respectfully submit that nobody really knows what’s going on in these ligaments. Since collagen molecules themselves do not permanently stretch, we’re probably looking at something that happens between molecules, fibrils, or fibers. Perhaps cross-linkages between adjacent fibers break and reattach further down the chain. You might be able to stretch collagen fibers just like you can stretch a rope. You can make a little progress by pulling some of the fibers slightly past one another, but after a while you kind of bottom out and no further elongation happens without applying insane force and risking breakage.

Perhaps that’s what newbie gains are all about; they’re just like stretching a rope or a piece of string. Pulling at reasonable force gives you some quick gains. But beyond that, it seems to me that something else has to occur. I think that people who can make sustained gains are able to get their bodies working for them, rather than against them. Some combination of exercise, rest, and who knows what else coaxes the cells to replicate and/or to produce more meat (i.e., collagen). As new collagen is secreted, it works its way into the existing tissue structure, possibly allowing it to elongate.

The IPR hypothesis presented by Shiver, MX, Xenolith, and others, was based on this idea. They said the exercise causes inflammation, which begins a cascade of healing responses, which include proliferation and remodeling. Proliferation involves connective tissue cells (fibroblasts) secreting procollagen into the intercellular ground substance. That procollagen matures into collagen (type III, I think), which works its way into the tissue matrix, thus adding “meat” to the structure. If you’re lucky, and maybe if you structure your PE routine correctly, that new meat will add to your penis along the desired dimension.

I respectfully request that you reread the definition from Dorland’s Medical Dictionary. It said that hyperplasia is: “…the abnormal OR increase in the number of normal cells in normal arrangement in a tissue.” (My emphasis added). What does the word “or” mean to you; to me it means one or the other.

Let me let you read some exerpts from medical textbooks that disagrees with your statement.

The area of medicine with the greatest experience with connective tissue is Orthopedic Surgery. Here is a reference from “Current Diagnosis & Treatment in Orthopedics”, 4th Edition, Harry B. Skinner. Chapter 1. Basic Science in Orthopedic Surgery, Ranjan Gupta, MD, Vincent J. Caiozzo, PhD, & Harry B. Skinner, MD, PhD. This concerns ligament repair:

“Biologic Tissues in Orthopedics
Healing Mechanisms

During tendon and ligament healing and repair, fibroblastic infiltration from the adjacent tissues is essential. The healing events are initiated by an inflammatory response, which is characterized by polymorphonuclear cell infiltration [white blood cells], capillary budding, and fluid exudation [oozing] and continues during the first 3 days following the injury. After 4 days, fibroplasia occurs and is accompanied by the significant accumulation of fibroblasts. Within 3 weeks, a mass of granulation tissue [healing tissue] surrounds the damaged tissue. During the next week, collagen fibers become longitudinally oriented. During the next 3 months, the individual collagen fibers form bundles identical to the original bundles.”

And there’s this from “Current Surgical Diagnosis and Treatment”, 12th Edition, Gerard M. Doherty and Lawrence W. Way. In Chapter 6. Wound Healing, Thomas K. Hunt, MD:

“Fibroplasia & Matrix Deposition
Fibroplasia

During the course of healing, fibroplasia (replication of fibroblasts) is stimulated by multiple mechanisms…

Dividing fibroblasts are seen mainly near the wound edge, where they are exposed to the growth environment…

The fibroblasts secrete the collagen and proteoglycans of the connective tissue matrix that weld wound edges together.”

Fibroplasia is hyperplasia (increased cell division) of fibroblasts, the cells responsible for the production of the proteins (for example, collagen) that make up connective tissues of which the suspensory ligaments and the tunica are composed (though of relative different composition from one another).

I know it is difficult to obtain medical references if you either are not associated with a medical library or don’t have access to their online electronic resources. I do. I tend not to get mine from Wikipedia. Even though it may sound like it, I am not trying to be arrogant or elitist by saying this, but I have better sources and I don’t trust an online encyclopedia that can be altered by anyone.

This represents hyperplasia in muscle which is not related to connective tissue for this discussion

I will agree that all of your examples are evidence of abnormal hyperplasia. But as I said above, you have excluded normal hyperplasia, which by the way does exist.

It is clear that I disagree with your contentions regarding hyperplasia (in this case fibroplasia) as a mechanism of repair of connective tissue. I present evidence from respected medical sources regarding repair and healing in connective tissues that does involve hyperplasia so that the cells (fibroblasts) can repair or increase connective tissue volume (due to injury or overloading, such as hanging) by increased production of the connective tissue subunit proteins. I hope that this makes my understandings clear. If you have any other medical sources to dispute this. again, I’m listening.

Pudendum I agree with you but what is the secret ingredient? How can one increase this potential of hyperplasia. And how does telemeres play a role in this.

There is a very long, complex but good review paper in Physiology Reviews 2004;84:649-698, MICHAEL KJÆR, “Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading”. It concentrates on tendons, but they have close similarities to other connective tissues (like ligaments), though they have less elastic component.

The author reviews a number of suggested mechanisms for the increase in fibroblast numbers and the stimulation of them to make and secrete connective tissue subunits involved with remodeling injured connective tissue. Loading of a tendon (by increased muscle stretch) causes connections between fibroblasts (through what are called gap junctions) to be broken. The loss of the “communication” (cell signaling) between the cells causes the fibroblasts to reproduce.

They also respond to the growth factors released by white blood cells and other garbage eating cells (macrophages) that enter the area after injury.

I found this information regarding those illusive and not well understood telomeres in the “Review of Medical Physiology”, 22nd Edition, William F. Ganong, Chapter 1. The General & Cellular Basis of Medical Physiology:

“Telomeres

Cell replication involves not only DNA polymerase [enzymes that make DNA copies] but a special reverse transcriptase [make DNA from RNA, not the normal way of RNA from DNA] that synthesizes the short repeats of DNA that characterize the ends (telomeres) of chromosomes. Without this transcriptase and related enzymes known collectively as telomerase, somatic [body] cells lose DNA as they divide 40–60 times and then become senescent [quiet] and undergo apoptosis [cell self-destruction due to damaged DNA]. On the other hand, cells with high telomerase activity, which includes most cancer cells, can in theory keep multiplying indefinitely. Not surprisingly, there has been considerable interest in the telomerase mechanism, both in terms of aging and in terms of cancer. However, it now seems clear that the mechanism for replicating chromosome ends is complex, and much additional research will be needed before a complete understanding is achieved and therapeutic applications emerge.”

[Text in brackets are translations of medical terms made by me]

In Harrison’s Principles of Internal Medicine, 16th Edition, Part 3: Chapter 57. Chromosome Disorders:

“…[telomeres] are important for allowing DNA replication at the ends of the chromosomes.”

There are theories out there that there are a finite number of divisions by cells and that this may play a role in aging. Telomeres may play a role in this. Interesting.

Addressing…
#1: How could you possibly know this?
#2: I masturbated almost after every PE session - and I went from 6.12 x 5.25 to 8.18 x 6.4+
#5: I’ve gone more than 14 months off - Cold Turkey - and I’ve lost very little (maybe 1/8" erect in both length & girth); furthermore, I don’t appear to continue to lose gains. Are you suggesting that my cells are still being "rebuilt"….after 14 months rest?
#7: Is easily explained by the simple truth that beginners are furthest away from their own ultimate potential; hence, there is a greater margin for error and a lot of ground to make up. You see this type of "honeymoon" progress in all areas & endeavors - even those unrelated to sports/muscle building, etc.

What you are suggesting, in fact (tissue repairs, cells rebuilt) sounds much like hypertrophy - which is exactly why the medical profession denies that NPE is real (on that grounds), because the penis is not comprised of striated skeletal muscle…and the type of thing you’re describing just doesn’t happen. And they know this.

I’ve constantly heard doctors and others say, "You can’t make the penis larger through exercise - it’s not a muscle." However, I’ve never heard them address PE gains through the lense of plastic deformation. I believe that if they did this, they’d no longer deny that NPE is legit.

I was heavily into weight training in the past, and I packed on a lot of muscle. Over time, I drifted away from the gym……..and my muscle mass drifted away from me. That’s because muscle mass IS "built up" - it’s not the result of plastic deformation. However, I’ve lost so very little of my PE gains (and it’s possible that I had not even fully cemented the gains that I listed as my best - hence, I didn’t "have" them to lose). If that’s the case, then I lost even less than 1/8" on both ends.

If you're theory were correct:

1) PE is not permanent at all - but must always be vigorously performed or your gains disappear - necessarily.

2) Over the past 14 months off, cold turkey, I should’ve lost AT LEAST 50% of my gains - yet, I didn’t even lose 10% of my gains (perhaps even less had I not cemented my best measurements prior to stopping).

3) The medical profession would’ve embraced PE as readily as they’ve acknowledged weight training.

In fact, I could’ve only retained my gains if they were the result of plastic deformation (of which I’m certain they are). Since I ain’t doin’ any "rebuilding," yet my size remains. If only that were true of my pecs & arms. :(