For Science minded PE'ers

Okay, those of you who know me will be aware that I’m always up to some off the wall scheme or other, trying to understand what the parameters and limitations are with regards PE.

I’ve looked at Pro-hormones, heat, uncouplers, collagenase, prostaglandins, and of course exercise routines.

Today I want to propose an idea based on seemingly innocous comments made by various people here over the years, and combine it with another area of study I’ve recently been exploring as a result. This may ramble on a bit (I’m not sure until I’ve finished writing), but I will get to the point eventually. But first, here are a two generalisations I’ve heard mentioned:

1. Some people seem to be genetically gifted, while others can’t gain much no matter what.
2. Some people notice that they gain better when on a diet, others claim this is untrue.

While it may well be true that some are genetically gifted, or others notice better results from diet, I would like to propose that while the cause may be different, or the outcome different, the result could be traced to the same response, and possibly (at a push), even be predictable.

It is known that different body types react differently to diet. For example: Some people have a real hard time on a low/no carb diet suffering from lack of energy, whereas others can function just fine (the eskimos amongs us perhaps?). A diabetic (Type I or II) person has to take great care over their diet in order to manage their blood sugar and keep it within certain tolerances. Yet another person may eat simple carbs and fast food their whole life and never get fat or insulin resistant.

Diet response is partly genetic and partly lifestyle. For the puposes of the rest of this post I want to blur the two, and just say that it is about sugars.

Using the example of a diabetic person, they have at times, very high glucose levels in their blood. This results in Advanced Glycation Endpoints (or AGE). The simple description of this is that it produces accelerated cross-linking throughout the body, resulting in increased thickness and stiffness of tissues. This results in reduced capacity of arteries, increased renal loads an inefficiency, retinal/cataracts disorders, capilliary restrictions, vascular rigidity, skin remodelling to primarily type I collagen causing thinness, wrinkles etc. which means that the collagen is less soluble, and less digestible to collagenase, pepsin. It’s not just diabetics that get this, we all do (just not normally as quickly). It is one of the greatest limitations to longevity (the other two biggies being telomere shortening and oxiditive stress).

When we PE we cause the crosslinking in the tissues stressed (regardless of whether it is AGE induced or not). The body responds by making them thicker, stronger and of course more stiff. I believe this is why most of us see great newbie gains, but as we continue we must add more workload only to see progressively diminishing returns.

Many find that by taking a ‘deconditioning break’ we find that we can suddenly make some fast (if short lived) progress, before again hitting plateau. I would suggest that the body is able to slowly repair these cross links through normal cell turnover (which in most type I collagen is very very slow, except of course in times of growth such as puberty, where hormonal profiles encourage huge turnover of tissues). The long half life of collagen makes it susceptible to acumulating molecular lesions and axial structure changes that ‘rapid turnover’ tissue don’t have time to suffer. The addition of crosslink inhibitors can help here (more of which later), but the resulting progress depends on crosslink formation versus crosslink repair, and in most cases of modern lifestyle/diet, this ratio is very poor - if not in the negative.

But what if we could not only inhibit these cross links, but we could also actually break existing crosslinks? Well, believe it or not, that possibility is actually on the horizon. There are at least 375 different compounds that may have this ability to a greater or lesser degree, and on different tissues, but for the purposes of this thread we’ll stick to what we actually have a chance of getting hold of, even if it’s not the best tool for the job. In fact I’m only going to mention two products, as these are what I consider the best of the bunch in combo, but if you want to persue your own studies there are many (many!) more.

Carnosine: Widely available amino acid that is known to inhibit cross linking. In simple terms, where a crosslink is able to occur, the carnosine is very effective at tying up one end of the link, rendering it inert. It has the added side benefit of being a pretty good anti-oxidant, and recommended by many organisations such as LEF.

Algaebrium Chloride: Like most crosslink breakers, this is actually a type of salt. It is very effective at breaking ‘ill-formed’ links (loosely speaking, those that are not protein to protein), but does not affect healthy tissues. This means that is can reduce unnatural wall thickness and remodel tissue type of most major organs, and effectively turn back the clock on crosslink damaged tissues. It is not the be all and end all of crosslink breakers (which will probably be a mix of several types for different purposes), but it appears to be quite effective and non toxic in all studies to date, including human trials in the US (Altheon corporation). It can break a crosslink without rendering itself inert or spent, but the downside is that there is nothing to prevent the crosslink from reforming. Algaebrium chloride (AC) can of course break the link over and over, but the real beauty of this is in combination with Carnosine. The AC can break the link, and the Carnosine can be the sacrificial supplement to bind it. Studies show good improvements (40%+) in only a few weeks/months in mogril dogs with AC alone.

Here’s one final bit if good news: Both Carnosine and Algaebrium Chloride have extremely low molecular weight (300-350 daltons), which means both would absorb very well in even a very basic transdermal. That’s not to say that a transdermal is the only way. These are both orally bio-available, and who knows, it might have a huge positive impact on you health(?)
Perhaps (and I don’t want to cause unecessary optimism here because it is just pure speculation) if we can prevent, reduce or even reverse crosslinking to a fair degree, then we can start to see gains like we did as newbies. Then again, perhaps it won’t work at all, and in 6 months time I’ll be writing about another snake oil half-baked proposition :) I don’t know, and I’m just throwing it out there as food for thought with the hope that a few other minds might become interested and bring something to the table.

Regards

Shiver

There should not be such confusion with the simple principles involved in an erection and the way to make it larger. It is all about blood volume and the size of your vascular infrastructure. Due to genetics some people are born with traits that lead to a larger vessel, these people are way ahead of the average guy because they have a bigger balloon hanging off their body. Now, how to make a bigger balloon when you are stuck with a baby balloon. Well, if you have a martini straw feeding your balloon your not going to be much of a challenger; but if you have a fire hose you are going to be a worthy competitor.

The reason you gain growth quickly in the beginning is because you have unused elasticity in the chambers that form the penis and by exercising or jelqing you create stretching or expansion quickly of this very elastic physiology. So, even though you have martini straws feeding your balloon the jelqing has created additional volume for your penis to expand. It is not unlike stretching a new balloon in your hands to make blowing it up easier. These initial forays into PE are the easiest gains to make, it is like sack stretching, you can see very quick gains in increasing the surface area of your scrotum. Skin and some other soft tissue respond very quickly to stretching, they permanently deform in a matter of weeks.

The reason gains begin to slow down is a result of the difficulty affecting other anatomy; namely, the blood supplying system to the penis. Bigger pipes will result in a bigger boner, it’s that simple. It is a slow process to increase the diameter of your veins and arteries. Since it would be uncomfortable to hook-up a pressure hose to your willy you have to do the exercises necessary to increase the volume of blood to the penis. Most people when they start this game have a smooth lilly white penis with little martini straws under their skin, you have to replace that wimp-ass system with high capacity pipes.

So, instead of doing the worthless exercises, do the ones that promote the expansion of your arteries and veins to maximize your potential. Expanded pipes will big up your trout and add length. It’s all about the blood.

What stops those straws from continued growth though?

Everything I’ve read over the years suggests that it is fibrosis. This replaces elastin with collagen (mainly type I).

“Make it as simple as possible, but not more so” :)

stevie31 - In Need of Girth

Shiver,

Very interesting stuff.

I’ve recently started hanging. Many threads attribute gains from hanging to talk stretching/breaking connective tissue fibers, and then holding the penis in an extended state (via ADS) while the fibers repair.

But some things I’ve been reading recently (here and elsewhere) suggest that it’s the lateral connections between fibers that are responsible for growth, not the fibers themselves.

This may be a matter of semantics, since connective tissue comprises a hierarchy of “fibers,” from single collagen molecules to layered bundles of the same.

The basic idea that’s been coming through is that the lateral connections between fibers (your “crosslinks?”) “let go,” thus allowing the fibers to slide relative to one another and reconnect laterally at different points. It’s not that the fibers themselves stretch or break (at least not the molecular fibers), its simply that they reconnect more remotely, i.e., in a way that allows the overall structure to lengthen.

Are the cross-linkages you refer to the mechanisms that make the lateral connections between collagen fibers? Are we talking about the same thing?

If so, I can certainly see the benefit of playing with the biology of forming and breaking these crosslinks in promoting gains.

For the benefit of non-biological sciences types (like me), could you please explain exactly what these “crosslinks” are and exactly what structures they link together.

Thanks!

It seems that fibrosis will only let us gain so much and then that’s it! How can you expand without elastin?

I thought elastin was what made the penis contract?? Collagen forms the tough structure that limits the length and elastin causes it to shrivel up. No??

I’ve read at Thunder’s before the theory that Vitamin C in high doses should be avoided because of it’s ability to cause increased collagen. I’ve taken Vitamin C in 1000mg - 20000 mg per day for the last 17 years ( and haven’t had the flu or a cold in the last 17 years) and still have managed gains since beginning pe. Perhaps it has slowed me down? But I also have taken fish oil capsules for many years now and perhaps this increases elasticity? Ok, I’m confused now.

Shiver,

I see you mentioned LEF in this thread. Though I’ve never joined their organization, I’ve been reading their great monthly magazine for many years. Your mention of telemere shortening caught my eye also. Have they found yet any natural supplement to take orally for slowing down or even re-lengthening telemeres? I don’t always read the magazine from cover to cover anymore, so perhaps I’ve missed new information concerning this.

Let me preface all this by saying that the text below is only the mental model I have at present. It is not a fact, and anyone who knows better than me is welcome to take part in changing or debunking any part of it. I’m not a professional in any related field, just an enthusiatic amateur. Onwards…

I cannot speak from experience regarding hanging as I never wanted to lengthen my ligs. If I ever start hanging it will be out of desperation because I’ve run out of ideas on extending the tunica :) That said, I would generally go along with the above for a simple working definition.

First let me qualify that I don’t really understand what lateral connections are, since it implies an axis. I envisage 2 layers of connective tissue that make up the tunica (longitudinal and circumferencial). For the purposes of a taxonomy we’ll call them one and the same unless someone can correct us. But to answer your question I’d say yes…and no.

I say Yes because fibres can slide past each other to a limited degree. This is especially so with Heat in the correct range (as discussed in the IR heatpad experiment). A collagen matrix extended with heat induces plastic deformation much more so than at normal body temperature, with the added benefit that it does so with much less damage than at normal temperatures. The extensibility however is limited by the construction of the cellular matrix. A technically inaccurate but easy model to imagine and describe this is if you picture a crosshatch pattern made from wooden strips, with pins at each intersection (like a wall trellis). The pins have a heat sensitive glue to stop them moving. If you apply heat it melts the pin glue and allows you to deform the trellis to make it longer, and when it cools down it resets the glue without doing much damage to the wooden strips. Despite that each sheath is separate and has a general axis bias, they do (in my experience at least) affect each other. I can get length gains with heat, then if I try to get girth gains, it is at some (but not complete) expense of the length gains, and vice versa. I don’t know if anybody else has had this observation.

The reason I say No is because if you want to extend beyond the plastic deformation limits of the above wall trellis analogy you need to break the strips of wood little by little, and the body will repair them. More breaks and reconnections over time will allow this trellis to grow slowly longer, where all the limiting wooden strips need to be broken, but bit by bit, where the weakest go first, then the next weakest etc. As for crosslinks in this analogy, imagine that the body doesn’t just fill in or lengthen the strips of wood, but it also nails down some additional new strips across the planks, which effectively triangulate the structure of sorts. What this will do is add more strength (more fibres) to the structure, but it will also add rigidity/stiffness. On top of that it will prevent retraction of the penis (hence increased flaccid length).

Elastin and collagen are intermixed. When repair/remodelling takes place, the body will signal a disolving of damaged tissues, which reduces includes elastin. When the body strengthens tissues, it does that only with type I collagen. I believe TGF-B1 (Transforming Growth Factor Beta-1) is the primary mediator here.

The proposal is that if we can get the above strips to break/lengthen/repair, but stop the cross braced wooden strips, then in theory we could avoid diminishing returns. But it is after all, just a theory.

I would keep taking the vitamin C if I were you since it provides for much more important things than PE. The rationale behind it is that lack of ascorbic acid will result in scurvy, which makes the collagen bundles weaker and brittle. It might help gains with PE, but at what cost the the whole?

I don’t get the LEF magazine (but I’d be interesting in a link to it). The only thing I know about limiting telomere shortening is MitoQ, and I don’t know much about that either. I believe it is a derivative or modification of idebenone that is around 200 times more active than idebenone (orally available), but there are limits and complications.

1. It (MitoQ) is limited in it’s activity to certain parts of the mitochondria (don’t ask me any more detail than that or I’ll fall flat on my face :)
2. Idebenone in vitro it was shown that while it did help limit telomere shortening, it was also a potent superoxide generator, which means it causes as much trouble as it solves. However, invitro these observations were not made.

Shiver,

I’m afraid I might be breaking forum rules by posting their link. I really need to learn the rules better. To be on the safe side I’ll PM LEF’s website to you.

I have for, what seems an eternity, been spouting this very observation.

Whenever I have made a significant length gain, it has been at the expense of some girth. I have been lucky enough to keep my length gains coming on a fairly regular basis, but when I do target girth, my length gains slow or even stop.

As always, great stuff Shiver!

The loss of some girth with increasing length is a natural result and it occurs because stretching tendons also results in stretching arteries and veins. As this physiology elongates you will have a slight reduction in the diameter of your blood inlets thereby affecting the flow characteristics of engorgement. Limb lengthening is not a new science and has been around since the 50’s, there is a direct correlation between the length of a tendon or ligature and the resultant permanent stretch that can be attained. The suspensory structures of the penis are relatively short and this fact constricts the theoretical limits of elongation that can be achieved.

I see these posts of individuals that lament their slow gains and they have already gained an inch. They don’t realize how incredible an inch is as it relates to the penis. I mean they do limb lengthening on the appendages of the arms and legs where an inch is considered monumental in most cases. Here again genetics plays a role and will ultimately determine size, shape, enlargement. Work on your pipes if you want your unit to appear on satellite imagery charts, you are over thinking this production.

Are you suggesting there’s a theoretical limit to how much some one can gain? Or, are you just proposing this as a short term condition?