How does Penis Enlargement actually work? A somewhat deep dive.

The following is a re-post of an article I wrote on Reddit's r/gettingbigger - and I am reposting it here because it is vital to understand what exactly PE is all about: 

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How does PE actually work? Like, on a cellular level? What exactly is happening in the tunica albuginea, the suspensory ligament and the erectile tissue? Let’s deep-dive.

I will assume some prior knowledge of cell biology, but try to make this as simple as I can. However, I hate holding back on using proper language, so please excuse some scientific lingo. You might even learn a new word or two...

Cross-section of the penis

 

I assume you know that we are primarily enlarging the penis by stretching the suspensory ligaments, the tunica albuginea and to some extent also Buck’s fascia (which, in addition to encapsulating the two corpora cavernosa (CC) and the tunica albuginea (TA), also constitutes the outer layer of the corpus spongiosum (CS), and transitions into the suspensory ligament, which is just a continuation of Buck’s fascia). We are also stimulating the production of more blood-holding tissue inside the CS and CC to “fill in the gains” and convert an increased flaccid length to actual increased erect length, as well as filling out any girth gains.

 

But how? Mechanotransduction and growth factors!

What exactly goes on in the tunica or suspensory ligament when we stretch it? And why does stretching cause growth? Are we making it thinner, as when a rubber band gets thinner the more you stretch it? Or are we causing it to grow thicker, and if so how? That’s what I will attempt to explain.

 

The “glue” that holds the various organs of our bodies together, which makes up the material between our muscles and our skin for instance, is called the “ECM” - the extracellular matrix”. In this, we have a lot of interstitial fluid, and many cells get their nutrients from this fluid and dump their waste products into it. The matrix itself is made almost entirely of sticky fibres of collagen - it’s like an open cell foam. This collagen is produced by fibroblasts - the same type of cell that produces the collagen in your fascia, tendons, ligaments, and most importantly for our purposes our tunica albuginea.

Fibroblast (a type of “mesenchymal stromal cells”, which is a subcategory of stem cells), as most other cells, have a soft internal skeleton, and this skeleton sort of protrudes through the cell membrane at special adhesion sites, and this is where cells attach to other cells and stick together. Here’s a quote from a study which explains it pretty well, but buckle in for some lingo…

“Cells can detect and react to the biophysical properties of the extracellular environment through integrin-based adhesion sites and adapt to the extracellular milieu in a process called mechanotransduction. At these adhesion sites, integrins connect the extracellular matrix (ECM) with the F-actin cytoskeleton and transduce mechanical forces generated by the actin retrograde flow and myosin II to the ECM through mechanosensitive focal adhesion proteins that are collectively termed the “molecular clutch.” The transmission of forces across integrin-based adhesions establishes a mechanical reciprocity between the viscoelasticity of the ECM and the cellular tension. During mechanotransduction, force allosterically alters the functions of mechanosensitive proteins within adhesions to elicit biochemical signals that regulate both rapid responses in cellular mechanics and long-term changes in gene expression. Integrin-mediated mechanotransduction plays important roles in development and tissue homeostasis, and its dysregulation is often associated with diseases.” (From: Integrin-mediated mechanotransduction, Sun et al Journal of Cell Biology 2016.)

 

Allow me to continue in technical fashion; Fibronectin is a high-molecular-weight glycoprotein of the ECM that fibroblasts produce. It’s involved in cell adhesion, growth, migration, and differentiation. Fibroblasts attach to fibronectin via integrins, which are transmembrane receptors that facilitate cell-ECM adhesion. This interaction not only anchors fibroblasts within the fascial tissue but also transmits mechanical signals between the ECM and the cytoskeleton of the fibroblasts, influencing cell behaviour and tissue remodelling. Fibroblasts also connect to each other directly through “gap junctions”, which are specialised intercellular connections that allow for the direct transfer of ions, metabolites, and other small molecules between cells. This communication modality is important for coordinating cellular activities across the tissue, including responses to mechanical stress and the regulation of tissue repair and regeneration.

 

Now again, but simplified:

Ok, that was a lot of complicated lingo, but the main thing to take away is that certain cells are sensitive to mechanical forces such as stretching. They register these forces and activate cellular machinery to respond - both short-term responses and long-term responses. Fibroblasts in the tunica and ligament will up-regulate the production of collagen. They go:

“Oops, that was a LOT of stretching my dude - in fact it was a little too much for comfort man - better make more collagen so that we can resist that kind of stretching in the future without taking damage in case you ever pull that hard again!”

In biology and medicine, this is called “adaptation”. The exact same thing can be observed in blood vessels, where repeated stretching stimulus can cause the production of more collagen to thicken the outer layer and to increase the internal volume to increase blood carrying capacity.

 

This whole process of up-regulating gene expression for growth is controlled by external and internal chemical growth factors. There will be an amount of inflammation to help recruit the immune system for clean-up and repair. There will be some amount (probably small, but I don’t know this for sure) of hyperplasia, i.e. production of more fibroblasts, and there will probably be some amount of cell growth (hypertrophy) of the individual fibroblasts for them to cope with the increased demand for collagen production. But more than anything, there will be more collagen produced. The exact cellular pathways by which mechanical stress causes this cascade of events that results in the release of growth factors “is not well understood”, as scientific studies often say - but we do know the result.

Several growth factors are secreted by fibroblasts in response to mechanical stress, including:

Transforming Growth Factor-beta (TGF-β), which is a key regulator of cell proliferation, differentiation, and ECM production. It plays a significant role in wound healing and fibrosis, promoting the deposition of collagen and other ECM proteins to strengthen the tissue. We don’t want fibrosis, which is just another name for scar tissue. If you pull so hard you get fibrosis, you’re on the path to developing Peyronies disease. But we do want some production of TGF-β for sure, which is what we get by pulling adequately hard but not too hard on our junk.

Fibroblast Growth Factors (FGFs), which are involved in a variety of processes, including cell growth, morphogenesis, and tissue repair. They can stimulate fibroblasts to proliferate and increase the synthesis of ECM components (i.e. collagen).

Platelet-Derived Growth Factor (PDGF), which attracts fibroblasts to the site of an injury and stimulates their proliferation. It also plays a role in vascular remodelling and can promote the synthesis of ECM components (again, collagen).

Vascular Endothelial Growth Factor (VEGF), which is primarily known for its role in angiogenesis (the formation of new blood vessels), but can also affect fibroblasts by promoting the formation of new blood vessels needed to supply nutrients to repairing tissues.

 

 

 

 

So, your tunica albuginea will not grow thinner as you stretch it. Instead, it will actually grow thicker. It will in fact grow so thick it will gradually get harder and harder to gain since its load-bearing capacity will increase. In the end, you won’t be able to pull hard enough to cause good growth stimulus with a vacuum cup, because that kind of pulling force would result in blisters. This is why it’s a good idea to take a hiatus now and then - a deconditioning break to let your tunica rest completely, where it gets a chance to grow thinner and more malleable again. This is also where people have experimented with chemical compounds to break down the collagen. It’s also where heat can be tremendously useful to soften the collagen and allow you to stretch your penis more than you would otherwise be able to.

 

Heat and collagen malleability

So, maybe let’s talk about heat for a while. Heat changes the properties of collagen. The penis is normally around 33-34°C, and at that temperature collagen is pretty stiff because individual strands of collagen called “fibrils” attach to nearby fibrils with hydrogen bonds. Pulling on collagenous tissue repeatedly in a consistent direction will cause hydrogen bonds to break and the individual fibrils to align in the direction of the force, where they are strongest. Heat helps break these bonds and makes stretching the tissue easier at lower weights. Instead of pulling with 10 lbs of force to achieve a certain elongation/distension, you might get away with using half as much for the same result. But you need to get it up to around 39-43°C, which can basically only be done with infrared heat or ultrasonic vibrations. Normal heat pads or warm rice socks would need to be unbearably hot to the skin for there to be any chance that your tunica gets to ~40°C. Many IR heat pads with visible IR diodes also have red light diodes, and 640 nm red light has been shown to increase collagen production in skin. It’s unclear whether it can reach all the way inside the penis to the tunica albuginea, but it’s quite possible that it can. If it does, this would be an added bonus. I urge anyone to read the thread “Hanging with FIRe” on Thunder’s Place if you’re interested in how all of this heat+collagen business works.

 

Growing erectile tissue - filling the sausage skin

But let's get back to growth signals again. The suspensory ligament and tunica albuginea, as well as the Buck’s fascia are all collagenous tissue (with some elastin an other proteins for added stretchiness). We now have a grasp of what causes them to grow. But a consistent experience in PE is that we will pull on our weeners for months on end without seeing much at all in terms of erect growth - all we see is a longer stretched flaccid. BPEL tends to lag behind BPSFL by 3-6 months at least.

 

This is where PervMcSwerve’s “sausage analogy” is apt: By pulling on (or inflating) your sausage you stretch the sausage skin, lengthwise or girthwise, but you don’t add any filling to it, so it won’t look bigger. You need to add more stuffing inside the sausage skin. The stuffing in this case is erectile tissue, which is vascular/endothelial in nature.

 

In order to grow more erectile tissue, we need to cause a significant release of the vascular endothelial growth factor (VEGF) I mentioned earlier. And here’s the thing: We know exactly how to do this! VEGF is released my many tissues in our body in response to hypoxia, which is a fancy word for lack of oxygen. VEGF is like a chemical signal that tells any vascular or endothelial tissue to start proliferating and growing. So how do we cause hypoxia inside the penis? Simple - just clamp it hard and let the clamp stay on for ten minutes. This will cause the blood trapped inside the penis to be depleted of oxygen, and carbon dioxide will increase, changing the pH. In response, VEGF is released by smooth muscle cells in the CC and CS as well as by fibroblasts and the endothelial cells in the small blood vessels, and the result is the growth of more blood holding tissue. You fill out your sausage. Your Vienna sausage becomes a Kielbasa and eventually, hopefully, a Falu sausage (see Swedish classic porn flick “Fäbodjäntan” for the pop culture reference).

 

The alternate hypothesis - micro tears.

Are these the only ways your pickle grows? What about "micro-tears" and healing? Well, all I can say is that we don’t really have a full understanding of the process. It might be that this old PE theory holds a grain of truth, but I don’t think the evidence is there. It would be super interesting to see some kind of detailed imaging study of PE. Perhaps MRI, CT or high-resolution ultrasound, perhaps performed in a vacuum pump under pressure, to see whether the “micro-tears” hypothesis holds up to scrutiny. I doubt it does. 

 

What about fatigue and strain?

Well, when you pull on a tendon with a “small” amount of force, it will spring right back when you release it, and be exactly as long after as before. If you pull on it a little harder, with “medium” force, and repeat this pull many times and let it go on for a certain time, it will not fully spring back to its previous length, but will stay elongated for a while. You will have “remodelled” it. If you pull on it with even greater force, you get into the danger zone where small tears will start to form - individual collagen fibres will rip. This will cause swelling and require a time to heal, and it will weaken the tendon’s load bearing capacity - i.e. you have sprained it. If you pull with even greater force, it will rip completely.

 

With PE, best practice is to avoid tearing your suspensory ligament and tunica albuginea. (Understatement of the century?) You also don’t want to be in the “toe region” of the tension/deformation graph. You want your tunica to be about 3% stretched/engorged after a session as compared to its prior length/girth (this is called “fatigue” in BD’s terminology), and to accomplish this you need to be at about 4-6% or perhaps a little more, while you’re in the device you’re using (called “strain”).

Then you can just hope that a small amount of this elongation becomes “locked in” and becomes permanent. I personally believe it’s not strictly necessary to achieve this target elongation/expansion in every session, but that you do need to achieve it frequently in order to see good growth. The matter is complicated by the fact that there are smooth muscle cells inside the tunica albuginea and that there is a connection to your nervous system. You need to be in a relaxed state for the tunica to elongate/distend well and not turtle too much after your session.

 

Penile nutrition for growth?

The fibroblasts in the tunica albuginea don’t have direct access to a blood supply. Instead they get nutrients only from the interstitial fluid in the areolar tissue outside it, and by diffusion from the corpora cavernosa. In order to produce collagen, they need good nutrient delivery, which you can accomplish by being erect often and by increasing flaccid blood flow. This is where taking a PDE-5 inhibitor (phosphodiesterase type 5) like Cialis or Viagra and/or L-Citrulline can help by helping with vasodilation through relaxation of smooth muscle cells in the vasculature of the CC. More blood flow = more better. If you eat enough proteins, there is no reason to further supplement with collagen or glycine, proline and lysine for that matter - you will only ever grow by fractions of grams per day, after all. The problem isn’t your nutrient status, but the speed of nutrient delivery - so focus on having good nocturnal erections and plenty of daytime erections as well, if you want to optimise matters. Citrulline and/or Cialis are your best friends in this respect. And being a horny goat, of course! :)

 

But what is a greater understanding of these processes good for?

That’s a good question. One thing it’s useful for, is that it can help us generate further hypotheses or guide us in the search for even deeper and more instrumentally useful knowledge. For instance, knowing about mechanotransduction, integrins and growth factors can help us ask questions about what kind of stimulus causes the best growth trigger. Is it extended periods of hard stretching, or repeated sharp tugs, or repeated slower tugs that trigger growth the most? In other words, are super short intervals of super high tension beneficial? Are minutes-long intervals better than seconds long? Are 2-minute intervals better than sets of 10+ minutes?

Well, the strength we pull or inflate with matters. So does the number of times we stretch. So does the total time we stretch. All of them are growth triggers. Each will have their own unique trade-offs. Pulling too hard is dangerous. Pulling for a long time causes your sessions to go on for a long time, and if you’re not using enough force that time is completely wasted (as with some low-tension all day stretchers). Interval pumping/stretching is very active, so unless you have an automatic pump with intervals capability you’ll be busy the whole time. As long as you use adequate force, both intervals and constant tension/pressure will work, but a combination of the two might be the best of both worlds.

Another question to ask might be whether it’s beneficial to pull in multiple directions during a single session. Does triggering stretch receptors on multiple axes cause a better growth signal than only using longitudinal or transverse force? Well, I think we can say with some confidence that we simply don’t know that (yet). Doing bundled stretches before pumping gives me better expansion than not doing them - but is it also causing a better release of the four growth factors? Some studies I have seen actually indicate this might be the case. Multi-axial stress seems to be preferable to uni-axial. 

Does it matter whether I go to 4% expansion or 8% after pumping? Are two 10-minute sets of clamping better than a single 10-minute set for hypoxia? Can I do hypoxia clamping 7 days per week as long as I stay at 10 minutes per set, or will this cause issues? These are empirical questions and we only have n=1 “studies” with inconsistent methodology and no control groups to go by. Bro-science, in other words.

But at least knowing some underlying theory can help us ask informed questions like this, and perhaps guide us to methods that work or studies that lead us to further insights.

Gentlemen - enough with the theory already - back to pulling on your junk!