Lets get some facts straight about the Vac Extender..

[dcreynolds Senior Member Find all posts View Profile Close dcreynolds]

That was because he did not use the device properly. It is a medically proven fact that extending leads to permanent gains in length and very mild ones in girth. NIH among others have done research on penile enhancement alternatives to surgery that are safer and possible more natural and effective.

I'm not so sure about that.
I remember once reading that article in "GQ Magazine" about the SizeGenetics extender.
The guy who tested it said he lost all gains in a few weeks time.
I have no idea how legit is that article/magazine though.

[dcreynolds Senior Member Find all posts View Profile Close dcreynolds]

Incorrect, again! It is permanent and it seems like your failure to gain has lead to your disbelief. It is proven, however, and through various medical journals and research conducted by very leading medical institutions as well as many members who have become apart of the research themselves. I am one of the later and a patient of a highly respected doctor that is involved in PE and is currently conducting a study on the ways to enhance it for safer body modification that will also lead to permanent gains.

Muscles of the body are not the same as the penis. Poor comparison.

There are two basic phases in penis enlargement, the first phase is collagen decrimping phase (often called the "nubie" phase) and the second phase is the remodeling phase (which we previously discussed). In the decrimping phase" the collagen fibers exist in waves rather than straight lines of fibers. As traction is applied, this results in a change of collagen fiber configuration from wavy to straight fibers. From the removal of this "slack" some gains can be made. This why it is easier to gain when you first start PE.

Instruments that can produce adequate decrimping traction would be the pump/watermate or extenders. The water mate you use will pull the crimps out in a period of several months, maybe less. My concern with you since you indicated prominent soreness is to avoid overdoing things, therefore I opted to eliminate the extender. My job as a coach is to teach you how to effectively and safely achieve gains. We want to avoid excessive activity that could lead to injury.

The answer is yes and no. The traction from the extender is mostly pulling the "crimps" or waves out of the collagen in the shaft and ligaments, with a degree of collagen remodeling consistent with the limited traction of the extender. It takes substantial traction > 7 lbs to actually induce significant collagen remodeling using more advanced techniques.

I have been a power lifter and a body builder for years. The body WILL NOT burn off all that muscle and while you may lose some gains you will NOT lose a lot of them. That is a myth and is debunked. My trainer, a 6 time world champion lifter, is proof of that. After an injury from the 1980's left him with joint replacements and not able to lift and yet he maintained most of his gains.

Muscle tissue that you build in the gym will remain because muscle increases the human metabolic rate and because of it, any fat that the body may have will be burned up for energy. However, this is not necessarily true for body builders (more on this later). Should a person leave the gym for a period over 6 months to a year, they will experience some decrease, but not all by any far stretch of the imagination. In fact, most people unless you are a body builder and will retain their gains they made in the gym because it is not water or bloated tissue, but in fact new muscle development. Most body builders are massive but have little strength to go with their size because all they are doing in inflating their tissue through lower weights with higher reps where a CrossFit trainer or a power lifting trainer will use higher weights with lower reps unless you are in a cutting phase or cardio type routine.

It is not permanent. Is not as easy as it sounds. The best way to compare, is to hypertrophy in skeletal muscle. When you go to the gym and workout your biceps for example, you are doing the same. Stretching the muscle to the point the muscle fiber breaks. The body repairs it, it grows bigger and stronger. Next time you do the same, the whole process repeat, and that's how muscles grow. But is unnatural. If you stop working out, the body WILL burn that extra muscle.

In the case of connective tissue is the same. You would think that an Olympic gymnast has bigger tendons and joint tissue from so many years of constant exercise. Well, yes he does. However, once he retires and is 60 years old, will never be able to do a split. Why? because the body returned that tissue to its genetically designed state.

That's why the only real solution is, again, Genetic engineering. The same way we were created, is the same way to fix and modify ourselves. They left us here raw, unimproved, full of genetic defects, we can fix ourselves and even more, we can have bigger cocks than they have. That would be hyperplasia. Cell replication. That is permanent, forever. With hypertrophy, you are growing what you have. With hyperplasia, you are growing what you dont have, besides what you already have.

[dcreynolds Senior Member Find all posts View Profile Close dcreynolds]

Figure A. Overview of the Anatomical Structure of the Penis. Reprinted with permission [1].
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* While all structures are of importance, please note the following structures. In the top plate please note the fundiform ligament, suspensory ligament, ischiocavernosus muscle over crus, ischiopubic ramus. In the bottom plate please note the syspensory ligament, corpus spongiosum, corpus cavernosum penis, and bulbospongiosus muscle. Please peruse the other structures.
The Anatomy of the Tunica Albuginea in the Normal Penis. [2]
I rewrote this scientific article so that it is more easily understood by a non-scientist as it is filled with scientific terms and descriptions. I feel that it is highly significant and is a must read for your repertoire of understanding the penis collagenous structure.
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Abstract. “The tunica albuginea of the corpora cavernosa is a bi-layered structure with multiple layers. Inner layer bundles support and contain the cavernous tissue and are oriented circularly. Radiating from this layer are intracavernous pillars acting as struts, which augment the septum (make (something) greater by adding to it) increase ( and provide essential support to the erectile tissue. The septum is originates from the inner circular layer of collagen coming together to form a “wall” thus dividing the corpus cavernosum into two chambers. Outer layer bundles are oriented longitudinally or lengthwise orientation to the shaft. These fibers extend from the glans penis to the proximal crura, where they insert into the inferior pubic ramus. There are no outer layer fibers between the 5 and 7 o'clock positions. Elastic fibers normally form an irregularly latticed network on which collagen fibers rest. In Peyronie's disease the well ordered appearance of the collagen layers is lost: excessive deposits of collagen, disordered elastic fibers and fibrin are found within the region of the plaque.”
Collagen Fiber Alignment. The human tunica albuginea is a complex structure, and is designed to be functionally compatible for the purpose of sexual intimacy. The collagen bundles are oriented either circularly or longitudinally with multiple collagen bundle layers able to slide against each other .The inner layer of collagen is finer, and has circularly oriented bundles which surround and penetrate the cavernous tissue. The coarser outer layers are directed longitudinally extending from the base to the glans. The overall shape of the penis varies, with the location determined by the surrounding tunica albuginea.
Figure 1. Artist's drawing of penis depicts dorsal and ventral thickening and struts.
Septum and Corpus Cavernosum. The septum dividing the two chambers of the corpus cavernosum (cc) is formed from the inner layer bundles. The median septum is complete proximally (the base area) and extends distally into each crus (areas of attachment) and are often incomplete at the glans. The inner layer bundles also send off perpendicular or intracavernous pillars that act as struts analogous to spokes on a bicycle Figure 2. The struts maintain intracavernous support.. The dorsal aspect (top) is fenestrated (having fenestrae or windowlike openings). “In summary, the inner layer has circular bundles that send off projections into the septum and thickened regions at the 6 o'clock position that represent the coalescence of bundles from both sides.”1
Figure 2 Intracavernous pillars between approximately 6 and 2 o'clock position. Note striation. Reduced from X25. Reprinted with permission. [5]
Ventral (bottom) thickenings. “The outer layer bundles oriented longitudinally (along the length of the shaft from base to glans)condense to form triangular ligamentous structures that we call ventral thickenings at the 5 and 7 o'clock position Figure 1. The intervening space (the ventral groove) houses the corpus spongiosum. Absence of longitudinal bundles between the ventral (bottom) thickenings allows the corpus spongiosum (cs) to expand without restriction.”
Longitudinal band thickenings toward the glans. Note that the longitudinal bundles are thicker on top (dorsally) these dorsal (top) thickenings bands are located at the 11 and 1 o'clock positions and ultimately extend into the glans distally as a single structure. These longitudinal bundles are located in the glans at the 12 o’clock position.
Dorsal thickenings at the base. When the dorsal thickenings are followed toward the base (proximally), they form the walls of the dorsal groove Figure 1, then gradually separate, anchoring the penile crura to the inferior pubic ramus. The longitudinal fibers from the lateral (side) aspect (1 to 4 and 8 to 11 o'clock positions) interdigitate with the suspensory ligament and fan out to join the adjacent ischiocavernous muscle (very important concept!).
Summary Thus Far. Hence, a circumferential ligamentous structure composed of ventral (bottom) and dorsal (top) thickenings and the lateral (sides) bundles is created, anchoring the penis to the ischial tuberosity (section of the hip bone behind the penis structure) immediately ventral to the pudendal nerve (one of the main nerve tracts coming from the sacral spine area) while providing the cavernous tissue with structural support.
Role of Elastic Fiber Mesh. The second structural component of the tunica albuginea is the elastic fibers that form an irregularly latticed framework on which collagen rests Figure 3A &B. In the penile shaft tunical elastic fibers and collagen are intertwined. However, proximally (the base) strands of skeletal muscle intermingle with outer layer bundles along the lateral aspect of the crus penis (interface of collagen fibers and IC muscle). The elastic network is present but with fewer fibers. The tunica at both ends (base and glans) where the inner layer bundles terminate, consists exclusively of collagen, reminiscent of ligamentous tissue.
Figure 3. A, woven elastic network shows undulating collagen bundles. Electron microscope/microscope images. .
This concludes a review of collagen structure of the penis. For more details please see reference 1 at the end of this paper.
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Collagen Metabolism
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In this article, I have printed the abstract and introduction with the article figures 1,2, and 3. I felt it unnecessary to rewrite it as it is relatively easy to read and can be accessed free. Unfortunately I was unable to produce a clearer illustration of Figure 2. You can access at no cost this paper in its entirety from Medscape: Medscape Access [3]
Abstract. The process of wound healing consists of an orderly sequence of events characterized by the specific infiltration of specialized cells into the wound site. The platelets and inflammatory cells are the first cells to arrive, and they provide key functions and signals needed for the influx of connective tissue cells and a new blood supply. These chemical signals are known as growth factors or cytokines. The fibroblast is the connective tissue cell responsible for collagen deposition needed to repair the tissue injury. Collagen is the most abundant protein in the animal kingdom, as it accounts for 30 percent of the total protein in the human body. In normal tissues, collagen provides strength, integrity, and structure. When tissues are disrupted following injury, collagen is needed to repair the defect and hopefully restore structure and thus function. If too much collagen is deposited in the wound site, normal anatomical structure is lost, function is compromised, and the problem of fibrosis results. Conversely, if insufficient amounts of collagen are deposited, the wound is weak and may dehisce. Therefore, to fully understand wound healing, it is essential to understand the basic biochemistry of collagen metabolism.2
Introduction. Collagen is found in all of our connective tissues, such as dermis, bones, tendons, and ligaments, and also provides for the structural integrity of all of our internal organs.[1,2] Therefore, because of its wide distribution throughout our bodies, it represents one of the most abundant naturally occurring proteins on earth.[3] In addition to its natural abundance, there are well over 1,000 commercial products on the market today that contain collagen and collagen enhancers. These products are represented by body and hand lotions, nail treatments, firming gels, wrinkle injections, eye pads, and even anti-cancer treatments to name but a few. In recent years, new high-tech wound dressing materials and skin substitutes have become available for the treatment of partial-thickness injuries as well as full-thickness and chronic dermal ulcers.[2]
There are close to 20 different types of collagen found in our bodies.[4,5] Each one of these collagens is encoded by a specific gene. The five major types are summarized in Table 1 . The predominant form is Type I collagen. This fibrillar form of collagen represents over 90 percent of our total collagen and is composed of three very long protein chains. Each protein chain is referred to as an "Alpha" chain. Two of the Alpha chains are identical and are called Alpha-1 chains, whereas the third chain is slightly different and is called Alpha-2. The three chains are wrapped around each other to form a triple helical structure called a collagen monomer (Figure 1). This configuration imparts tremendous strength to the protein. To understand the overall structure of the collagen molecule, think of it as the reinforcement rods called re- bar that are used in concrete construction. Indeed if one converts the molecular dimensions of the collagen molecule to measurements that we can relate to, the molecule when scaled up would measure one inch in diameter to approximately 17 feet long. Therefore, collagen is indeed nature's re-bar, because it is responsible for the strength and integrity of all of our connective tissues and organ structures. [2]
Figure 1.
The basic structural unit of collagen is a triple-stranded helical molecule. From Molecular Cell Biology by Lodish H, Berk A, Zipursky SL, Matsudaira P, Baltimore D, Darnell J. © 1986, 1990, 1995, 2000 by W. H. Freeman and Company. Used with permission.
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Figure 1.
The basic structural unit of collagen is a triple-stranded helical molecule. From Molecular Cell Biology by Lodish H, Berk A, Zipursky SL, Matsudaira P, Baltimore D, Darnell J. © 1986, 1990, 1995, 2000 by W. H. Freeman and Company. Used with permission.
Basically all of the collagens share this triple-helical molecular structure as described above. However, the various other types of collagens have slightly different amino acid compositions and provide other specific functions in our bodies. Type II collagen is the form that is found exclusively in cartilaginous tissues. It is usually associated with proteoglycans or "ground substance" and therefore functions as a shock absorber in our joints and vertebrae. Type III collagen is also found in our skin as well as in blood vessels and internal organs. In the adult, the skin contains about 80-percent Type I and 20-percent Type III collagen. In newborns, the Type III content is greater than that found in the adult. It is thought that the supple nature of the newborn skin as well as the flexibility of blood vessels is due in part to the presence of Type III collagen. During the initial period of wound healing, there is an increased expression of Type III collagen. [2]
Type IV collagen is found in basement membranes and basal lamina structures and functions as a filtration system. Because of the complex interactions between the Type IV collagen and the noncollagenous components of the basement membrane, a meshwork is formed that filters cells as well as molecules and light. For example, in the lens capsule of the eye, the basement membrane plays a role in light filtration. In the kidney, the glomerulus basement membrane is responsible for filtration of the blood to remove waste products. The basement membrane in the walls of blood vessels controls the movement of oxygen and nutrients out of the circulation and into the tissues. Likewise, the basal lamina in the skin delineates the dermis from the epidermis and controls the movement of materials in and out of the dermis. [2]
Type V collagen is found in essentially all tissues and is associated with Types I and III. In addition it is often found around the perimeter of many cells and functions as a cytoskeleton. It is of interest to note that there appears to be a particular abundance of Type V collagen in the intestine compared to other tissues. [2]
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Figure 3.
The intramolecular and intermolecular cross-links formed within a collagen fibril. Copyright 1994 from Molecular Biology of the Cell, Third Edition , by Alberts, Bray, Lewis, Raff, Roberts, Watson (eds). Reproduced by permission of Routledge, Inc., part of The Taylor & Francis Group.
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Figure 2.
The intracellular and extracellular events involved in the formation of a collagen fibril. Copyright 1994 from Molecular Biology of the Cell, Third Edition , by Alberts, Bray, Lewis, Raff, Roberts, Watson (eds). Reproduced by permission of Routledge, Inc., part of The Taylor & Francis Group.
Conclusion. Collagen metabolism is one of the most complex and highly regulated processes in our bodies. As we move forward in the future to design new strategies and technologies to treat the many challenging clinical problems associated with wound healing, we need to keep in mind how our connective tissues are assembled and how they are remodeled.[2]

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Mechanical Stretching Effect on Collagen Hypertrophy
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* The article indicates that collagen obtained from spinal tissue and subjected to mechanical stretching in vitro (in the test tube) resulted in increased transforming growth factor and hypertrophy of the collagen. This study is sufficiently analogous to penis traction such that it can provide light upon the sequence triggered by traction. In this case the collagen tissue was found in ligamenturn flavum cells obtained from the human lumbar spine from patients undergoing spine surgery. The tissue containing the collagen may be abbreviated LFC, a traction device was applied for 48 hours physically deforming the tissue cells. Production of transforming gowth factor increased significantly which in turn also increased collagen synthesis within the LFC tissue. The study than is sufficiently analogous to PE traction to suggest that traction will intuce molecular disruption, or bond braking setting up a growth phase event modulated by growth factors. This type of scientific literature begins to give us a picture of events that occur in a desired scientific format elucidation of stimulus response effect on collagen dynamics. (This I felt was a “smoking gun” journal article).
Abstrct: “We investigated the effect of mechanical stretching force on collagen synthesis and transforming growth factor-/3 1 (TGF-PI) production using ligament cells isolated from human ligamentum flavum in vitro. Ligamenturn flavum cells (LFCs) were isolated from human ligamenturn flavum obtained from patients who underwent lumbar spine surgery. The LFCs were subjected to a mechanical stretching force using a commercially available stretching device that physically deformed the cells. Collagen synthesis and TGF-PI production levels in the LFCs were then examined. Notable increases were observed in the gene expressions of collagen types I, 111, and V in LFCs subjected to mechanical stretching force. Production of TGF-PI by the LFCs also increased significantly by the mechanical stretching force. Exogenous application of TGF-PI was confirmed to increase collagen synthesis of the LFCs. This data indicated that mechanical stretching force can promote TGF-Dl production by LFCs, resulting in hypertrophy of the ligament.”[ 4]
The JES Extender Study
The JES Extender Study. This is one of the studies I am aware of that proves penis traction works, therefore I have included it in my discussion. In this study Jorn Ege Siana, MD based his idea, which was very original at that time (1998), that human tissue would respond favorable to traction and result in enlargement. This was his hypothesis. An extraordinary innovative device was invented to test this hypothesis. The inventor was Jes Bec Muller and it was called the JES extender. To prove their hypothesis, the device was developed to impose a maximum traction force of 1500 g or about 3.3 lbs. It consisted of two dynamic metal bars hinged to the ring, connecting it to the silicon-support, fastened around the corona glans at the distal end of the penis. 18 patients ranging from 23-47 years were selected. The treatment period was a marathon 12 hours daily 7 days a week 8 to 24 weeks with a follow up: every 2.weeks. After 24 weeks the participants were gratified with an average 24% increase in penis length. This is the one of the most credible studies, confirming the validity of their hypothesis. I have personally used the JES extender in 1999/2000 and gained 1⁄2” in 5 months and thus have experienced is validity.
Observations and Conclusions.
We can see from the above information that a clearer picture of the spectrum of collagen architecture and dynamics. We can draw conclusions based on the above. The collagen/elastin architecture of the penis is the limiting factor. Circumferential traction whether it is imposed on the penis circumference through vacuum, jelqing, squeezes, or other expansion moves or on the length through manual or mechanical stretching induces a stimulus response resulting in collagen hypertrophy (enlargement). The traction event causes molecular changes in the structure such as breaking of covalent bonds which in turn creates a chemotactic event activating and mobilizing the platelets and inflammatory cells which are the first cells to arrive., They provide key functions and signals needed for the influx of connective tissue cells and a new blood supply. These chemical signals are known as growth factors or cytokines. The fibroblast is the connective tissue cell responsible for collagen deposition needed to repair the tissue injury.
This process works in PE through the use of traction at a force sufficient to induce the above scenario required to break bonds, etc. A force as small as several pounds as demonstrated by the JES Extender will work finitely to increase length, however I suspect that the potential gains from the JES may be limited to the maximum force available. As in bodybuilding the force is probably proportional to the effect. One applies x amount of force, gains result, than accommodation occurs resulting in no further gains in collagen/elastin. It then becomes necessary to increase the force to exceed the accommodation threshold and generate next stage gains. Then accommodation sets in again and progression requires more force to exceed the threshold response and so on. Time is also a foctor but for the purposes of this discussion, I will keep this a constant though it will need to increase to some degree as well. Thus intensity and time are the parameters that are modulated for prudent progressive gains. Another point, as the penis is naturally a contractile organ, sufficient daily “maintenance” stretching logically must occur to prevent the collagen from healing in the contracted state. For example you perform an “intense” routine causing collagen hypertrophy scenario, maintenance stretching is subsequently indicated to insure that appropriate enlargement healing occurs in the extended state. A review of daily maintenance and threshold exceeding intervention combination and scenarios can be reviewed in a subsequent article.
I have attempted to provide REAL comprehensive insight from the above into collagen dynamics to help the individual gain useful knowledge in their PE progression. Part II will look at another
component of the penis in like manner giving insights as to the concepts and expectations of penile exercising.
References
1. Frank H. Netter, M.D., The Netter Collection of Medical Illustrations, Reproductive System, 1997; Volume 2, Page 9.
5. 5. 5 Hsu G-L , Brock GB , Martinez-Pineiro L , Nunes L , von Heyden B , Lue TF . The three- dimensional structure of the tunica albuginea: anatomical and ultrastructural levels. . Int. J. Impotence Res. . 1992;4:117 .
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7. Baek SR et al, J Elast 80:13–31, 2005. 8. Driessen NJB et al, Biomechan Model Mechanobiol.7:93–103, .....2008. 9. Humphrey JD et al, Math Models Methods Appl Sci 12:407–430, .....2002
2. Gerald Brock, Geng-Long Hsu, Lora Nunes, Burkhard von Heyden, Tom F. Lue -"The Anatomy
of the Tunica Albuginea in the Normal Penis and Peyronie's Disease" - J Urol. 1997; Volume
157, Issue 1, 276-281
3. Robert F. Diegelmann, PhD, Collagen Metabolism, Medical College of Virginia, Virginia
Commonwealth University, Richmond, VirginiaPosted: 02/04/2002;
Wounds. 2001;13(5) © 2001 Health Management Publications, Inc.
4. Tetsuya Nakatani Takashi Marui Toshiaki Hitora Minoru Doita Kotaro Nishida Masahiro
Kurosaka. Mechanical stretching force promotes collagen synthesis by cultured cells from
human ligamentum flavum via transforming growth factor-*‐β1. J Orthopaedic Res. November
2002; Volume 20, Issue 6, Pages: 1380–1386.
6. Balestrini JL, Billiar KL. Magnitude and duration of stretch modulate fibroblast remodeling. J
Biomech Eng. 2009 May;131(5):051005.

[not2big Senior Super ModeratorPEGym Hero Find all posts View Profile Close not2big]

Hey DC,
Nice and informative, but still a bit over my pedestrian mind to comprehend the details. I am currently using an extender and try to maintain the tension at 800 gr. Over the past four months I have been required to add a pair of 1/2 inch extender bars on two separate occasions in order to maintain my tension at 800 gr. If I read the article correctly, it seems that you should be increasing tension in order to achieve growth, Yet I have achieved growth (at least stretched flaccid growth) while maintaining the tension at 800 gr. Is my experience consistent with the tenants of the article? or should I be increasing the tension to 1200 gr or 1500 gr in order to achieve real growth?

As a side question, but related issue, I looked up the definition of tension on the internet and found that tension is defined as a pulkling force Plus an equal resistance force in the opposite direction. Since you mentioned that tension should be 1500 gr which is equal to 3.3 lbs, is the true force of tension at 1500 gr more comparable to a hanging weight of 6.6 lbs (pulling force of 3.3 lbs plus a resistance force of 3.3 lbs)?

[brandonW Junior Member Find all posts View Profile Close brandonW]

Hi DC,

Thank you for your very informative and detailed post. I am new to PE. I plan to print it out to read. But how come I can't see the figures mentioned in the article? Thanks for helping.

Best regards,
Brandon