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Collagen Considered

Yowza. I had certainly read much of that information before - but never consolidated and organized for easy digestion. Thanks Modesto…and Hobby.

Facia (tunica) is Collagen Type I.
Smooth Muscle is Collagen Type III.

I spent a good bit of my lunch break yesterday discussing the nature of connective tissues like Collagen Types I & III. “Official science” offers us very little information that is directly helpful to PE…but most of you already know that.

“Synthesis of collagen involves a cascade of biochemical modifications of the original building blocks. Many enzymes, cofactors and growth promoters influence these modifications which are crucial to the structure and function of mature collagen. The most abundant form of collagen, Type I, consists of three units of polypeptide chains, which are comprised of subunits of amino acids. Differences in the chemical structure of the polypeptide chains determine the different collagen types. These chains intertwine in a triple helix to form molecules called procollagen. Procollagen is formed within the cell and subsequently transported outside of the cell into the extracellular matrix. Outside the cell, procollagen is altered to form tropocollagen, which is then able to form into microfibrils. Microfibrils form fibrils when they are packed together in an overlapping fashion. The microfibrils are held by hydrogen bonds, hydrophobic interactions and reinforced by cross-links between tropocollagen molecules. The characteristic types and amounts of their cross-links largely determine the mechanical properties of collagen fibers. As we shall see throughout this article, nutrient deficiencies and pharmaceuticals may influence synthesis or metabolism during the critical stages in development of collagen.”

Bingo. Now what?

“Ground substance: The ground substance fills the spaces in-between the cells and fibers. Its viscosity acts as a lubricant due to the high water content. Soluble precursors of the fibrous proteins, proteoglycans, glycoproteins and other molecules secreted by cells are abundant in the ground substance.”

Is this where our biomechanical growth starts? I’ll bet it is. Tensile forces such as those associated with PE trigger changes all along the collagen spectrum.
We should all be drinking plenty of water.

“Individual cells, such as the fibroblasts in connective tissue, rarely divide into new cells unless the tissue requires additional cells as when a tissue is damaged. During inflammation and repair, the numbers of fibroblasts increase within some connective tissues. The extracellular matrix greatly influences function and differentiation of the cells. Tensile forces may also influence cell function, as changes in cell shape may alter the responsiveness of the cell to hormones and growth factors (3). The discussions on inflammation and pharmaceuticals examine the influences of hormones and growth factors on cell function.”

Yup. Yup. Uh-huh. *Goon nods his greying head excitedly*

“Synthesis and degradation of tissues is a continual process and are integral parts of tissue remodeling and turnover.”

“Changes in gene transcription and in events after translation of macromolecules can alter distribution and deposition of tissue proteins and proteoglycans. For example, many pathological conditions are attributable to abnormal or insufficient collagen synthesis, such as scurvy and vitamin C deficiency.”

“Specific enzymes initiate degradation of macromolecules. Collagenases, which degrade collagen fibers, are synthesized by various cell types and stimulated by hormones, prostaglandins, and other substances secreted by lymphocytes and macrophages. Metal ions, such as calcium, also regulate collagenase activity. Enzymes within cellular lysosomes degrade proteoglycans. We will see how synthesis and degradation are an integral part of tissue turnover.”

“Proteoglycans in the extracellular matrix appear to regulate remodeling of connective tissue by influencing collagen formation during the repair process. Remodeling is also regulated by mechanical stimulation. Mechanical tension and compression modify bone and cartilage remodeling, where tissues such as these depend on diffusion of nutrients for maintenance since they have no direct blood supply.”

No direct blood supply? Hmmm. I’m thinking transdermal ointments…

“Turnover of connective tissue is the net balance between synthesis and degradation of the macromolecules. A turnover negative balance is characteristic of several inflammatory and joint diseases where degradation occurs at a higher rate than synthesis.”

That’s bad. It leads to Negative PI’s like shrinkage!!!

“The repair process in tissue injury involves managing macromolecule turnover so that synthesis equals degradation.”

And that is tissue maintenance or “the status quo” which, in my opinion, is also bad…er, NOT “desirable”. You understand.

“Turnover rate of various connective tissue components varies. Elastin may take months to years for renewal. Collagen is also a stable protein and renewal is slow. Replacement of mature collagen can require weeks to several months. Collagen turnover rates vary in different structures. Tendon collagen renewal is very slow, whereas the collagen of loose connective tissue that surrounds our organs is renewed more rapidly.”

THIS is where the IPR protocol shines the brightest. Rest gives the tissues the time they require to repair themselves. But How Much? What about BUILDING vs. just maintaining? Ugh.

Inflammation Phase:
“Acute inflammation phase: Immediately after injury, several vascular and cellular reactions initiate the response known as inflammation. The process begins with a release of chemical mediators from cells into the extracellular fluid. The initial tissue damage stimulates release of histamine from mast cells, which causes dilation of blood vessels in the local area and increases vascular permeability. Increased blood flow and fluids and proteins that leak from the permeable blood vessels cause edema in the tissue and consequent swelling. Cells migrate from nearby blood vessels and cause release of more inflammatory mediators, such as kinins and prostaglandins (PGs). Local tissue pressure and some of these mediators act on nearby nerves to cause pain. These events lead to the classical signs of inflammation: redness, swelling, pain and heat.”

“The primary purpose of inflammation is to rid the site of damaged tissue cells and set the stage for tissue repair. Acute inflammation generally lasts from 48 to 72 hours after an injury and gradually subsides as the repair process progresses. Many of the events that occur during this time initiate tissue repair. PGs are considered important mediators of inflammation and are often the target of intervention with anti-inflammatory agents. However, PGs may also have a significant role in tissue repair. Many immigrant cells also have significant roles in tissue remodeling. Leukocytes (white blood cells), such as neutrophils and monocytes, accumulate within the damaged tissue along with resident macrophages. Enzymes released from these cells help digest necrotic cells and degrade matrix molecules; neutrophils and macrophages engulf cell debris. Blood platelets release growth factors that stimulate new fiber and matrix molecule synthesis.”

Inflammation…good. Make it burn, baby.

Proliferation Phase:
“Matrix and cellular proliferation phase: Chemical mediators released by inflammatory cells stimulate migration and proliferation of fibroblasts, which participate in the repair process. Fibroblasts secrete fibronectin, proteoglycans and small diameter Type III collagen fibers. In addition to these fibers, newly formed capillary channels, clotting proteins, platelets and freshly synthesized matrix molecules form granulation tissue. However, this granulation tissue has little tensile strength.”

We NEED those fibroblasts. They create the new collagen tissues. Also, this may be the best time to apply a light tensile force, as the new tissues have little tensile strength and less force may lead to no new inflammation. (It could do more work.)

Remodelling Phase:
“Remodeling phase: Recall that remodeling reshapes and strengthen damaged tissue by removing and reforming the matrix and replacing cells. As repair progresses, inflammatory cells disappear, the number of blood vessels and the density of fibroblasts decrease. The proportion of Type I collagen to Type III collagen and the matrix organization increases. Collagen fibers are reoriented in the direction of loading, especially in ligament repair. Collagen matures and elastin forms; tensile strength increases. However, the remodeled tissue may not completely resemble the original and thus the mechanical capabilities of that tissue may be altered.”

But, the IPR protocol has already received much touting around here in the last year or so…the chemical manipulation of Collagen is what I am specifically after.

While it is CRUCIAL to get a better grip on the TIMING of IPR…I want to know more about how to increase the yields of the Proliferation phase.

If all we do is rebuild what was damaged…we have done nothing.

More later.


"Debate the idea..."

Originally Posted by goonbaby

If all we do is rebuild what was damaged…we have done nothing.

Right. If gains occur by manipulating factors associated with IPR healing, it is probably because traction biases the new collagen created during the proliferation phase to integrate itself into the existing tissue matrix in looser form. As more of the original, shorter collagen is replaced by looser collagen, the maximum extension of tissues (linear size) is increased.


Enter your measurements in the PE Database.

Originally Posted by ModestoMan
Right. If gains occur by manipulating factors associated with IPR healing, it is probably because traction biases the new collagen created during the proliferation phase to integrate itself into the existing tissue matrix in looser form. As more of the original, shorter collagen is replaced by looser collagen, the maximum extension of tissues (linear size) is increased.

Agreed. So, where I am focusing my attention is toward substances that can alter the state of collagen (and I still need to read more of those links you provided).

What I am thinking so far:

No single “PE gel” will do what we need it to. Clearly the body depends on many different (and sequential) chemical processes to repair damage or grow new tissue. Keeping in line with the IPR nature of collagen regeneration I propose at least two different “PE Gels” are required to coax collagen to rebuild along the desired axis.

Ointment #1: (Gently weaken tough collagen bonds & promote plastic deformation)
This substance would be used to soften the collagen bonds and retard the Inflammation response. Inflammation is a good thing…but I do not want too much too soon or the tissues may simply replace the damaged cells and stop.

Ointment #2: (Controlled Inflammation and mobilization of fibroblasts)
I want the collagen to relax and allow for some plastic deformation prior to triggering an inflammation response. Then I want the inflammation to be significant enough that it involves most of the tissues in the entire organ. I am still uncertain where the majority of new growth comes from so I want to involve as much of the shaft as possible.

Ointment #3: (Nutrient Bath & other “building blocks” for Remodelling)
This last ointment would work in tandem with some oral supplements as well, but generally speaking, I want to provide ample amounts of nutrient to dividing and developing cells.

My intuition tells me that the best time for these ointments to be applied would be before bed (best) or early in the morning (second best) after a nice hot shower.

Bear in mind, everything I am discussing here is theoretical (and certainly not new)…don’t be stupid and chafe about Goon urging newbies to whip up some snake oil. Someday I WILL do this…but I am not going to attempt it until I know much, much, more. Ok?

I have considered some of the ingredients for these ointments and I will list them below. Dosages have NOT been determined and I am keen on staying alive. I will work that out in detail with a “GP” and my sources will all be top shelf. ;)

———————————————————
Ointment #1 (Lavender Blend)

DMSO - Base/Carrier (Also effective anti-inflammatory and collagenase)
Vitamin E Concentrated Oil - Base & Support
Porcine Relaxin - Active Agent
L-Carnitine
Potaba - Support
PABA - Support
Verapamil - Main Active Agent ($$$)
Hydrocortisone - Support
Ibuprofen - Anti-inflammatory
Aloe - support
Iodine - Antibiotic
Lavender Essential Oil - vasodilator and fragrance
(adding scent will help identify different ointments)
———————————————————

Ointment #2 (Citrus Blend)

DMSO - Carrier (this substance is a terrific solvent for carrying other substances transdermally)
EMU Oil - Base & Support
Vitamin A (Fish Liver Oil) - Support
Vitamin C - Support
Zinc - Support
L-Lysine - Ginko Biloba - Support (circulation)
Aspirin - Support
Distilled Water - Base & Support
Hydrogen Peroxide - Support
Iodine - Antibiotic
Cirtus Essential Oil - fragrance
——————————————————-
Ointment #3 (Peppermint Blend)

DMSO - Base
Tribilus - Hormone Trigger & Support
DHEA - Hormone Support
Yohimbe - Vasilodilator
SupportL-Argenine - Support and Vasilodilator (studies suggest high dosages over short periods induce growth hormone release)
Taladafil - Triggers long-duration erections (<3 hours)
Bovine Collagen - Support
Glucose - Nutrient for diabetics (blood sugar)
BMP4 Protein - “Experimental” Support ($$$)
Hyaluronic Acid - Support
Forskolin - Support
Glucosamine - Support
Chondroitin - Support
Pepperment Essential Oil - Anti-inflammatory & fragrance
——————————————————

There are a few other substances I am considering but they are more dangerous and “experimental” as well as being quite costly. Safety is paramount, efficacy is secondary (but required) and cost is my last concern at this point.

I am developing this idea based on a rotating cycle of treatments.
Ointment #1 should give you about 2 good weeks of softened tissues before you should stop taking it. I expect there will be a two-three day “loading” period before the tissues are responsive. There may also be an equal amount of transition time required before you switch to ointment #2. So, I am building this idea on 21 day treatments of each ointment.

PE Strategy…
Using Ointment #1, I would do some significant hanging and stretching. The focus would be on linear deformation initially, but one should expect the lateral expansion to be possible as well.

Using Ointment #2, I would focus more on ADS work and intermittent jelqing. The majority of the “damage” was done during the first 21 days, so damage should be minimized or eliminated for the following 42 days. We are trying to get the tissue to respond as directed.

Using Ointment #3, (only at night for OBVIOUS reasons) was meant to take full advantage of the bodies natural rest & rebuilding periods. Since this period parallels the remodelling phase of IPR - we do very little active PE. Let the frequent and intense nocternal erections work that out. Lots of good engorgement with plenty of oxygenated and nutrient rich blood…that’s the idea anyway. 21 days of the best sex you have had in a while and then…reflect.

___________________________________________

Still with me Modesto?
Any thoughts so far?

(Please don’t call the cops.)


"Debate the idea..."

Goonbaby:

I admire your persistence and relentless pursuit to find the “magic” ointment that could alter the state of collagen. Please keeps apprised of your progress.

Originally Posted by ModestoMan
Right. If gains occur by manipulating factors associated with IPR healing, it is probably because traction biases the new collagen created during the proliferation phase to integrate itself into the existing tissue matrix in looser form. As more of the original, shorter collagen is replaced by looser collagen, the maximum extension of tissues (linear size) is increased.


Whoa, whoa,whoa…back the book mobile up there just a second.
Why would traction cause the new collagen to integrate itself into the existing matrix in looser form?
Are you guys hypothesising that by reducing the interstices (space between the matrix) during the proliferation phase, that once the loading is removed and the matrix regains its (somewhat) original size, the collagen will in fact be further apart and hence looser?
And ideally, wouldn’t we want the new collagen to be integrated into the matrix in any direction except parallel to the direction of loading and hence avoiding the new collagen achieving the highest tensile strength possible (that is, when the collagen is parallel to the loading)?

So if that’s the case, then the type of “traction” will differ depending on whether the PE’er is after girth or length.
If he was after girth, then use traction during remodelling so as to align the new collagen along the length of the penis, giving a reduced load capacity transversely, allowing easier girth gains.
If he was after length, then use all day clamping to remodel the collagen in the opposite direction, allowing easier length gains.

Hmmm. If that turns out to be correct…then YES, that is EXACTLY what I am saying. *cough*

A69, It’s hard to think with all that pounding and shouting. (LOVE the avatar!)

Doesn’t something like that makes sense? Modestoman is one sharp tack…and I have not intention of speaking for him when his PE-related knowledge base far surpasses my own. So I am speaking for Goon when I say that manipulation of the natural remodelling mechanism is not entirely understood and it may not be an intuitive thing. The fact is, I simply don’t know if this is correct…BUT, an illustration might help us all understand what we are talking about, A69.

If my focus was girth gains I might try clamping or heavy jelq, and erect bending routines. There is evidence around here to suggest these methods work, but the mechanism is not well understood - because they do not ALWAYS work and gain can be unpredictable even with a personal history of past successes.

Imagine the cellular structure of the phallic tissue could be represented as a grid where each living cell exists at the intersection between two lines. In a relaxed state, the cells are spaced evenly with negligible tensile forces in random directions. If we isolate the forces at play during erection then we can better predict how the tissues may react to applied forces in the flaccid state. Basically, ignore what happens when the tissue is erect. That is a natural function of the tissue and regular (natural) erections do not contribute significantly to PE gains. (Send all flames to ********…he is handling my hate mail these days).
Anyway, in the relaxed (flaccid) state the cells are stable and no biomechanical triggers are at work. There is some cellular die off and those are replaced by the body - but basically the system is in equilibrium.
Once we apply a significant tensile force (of unestablished degree) to the tissues along a single axis we strain the cellular matrix in primarily one direction. Our grid gets distorted in one direction more then the other while under load. The cells sense this and biomechanical triggers will begin the process of reinforcing the tissue to resist the perceived load. What the body meant for good - we meant for evil.
The new collagen will be constructed to support the existing matrix, but can it assume the load as long as the load remains constantly applied? Perhaps not. In a sense, the original tissues are still bearing the brunt of the load. If they FAIL, then there is some plastic deformation, and the new tissues will begin to assume loading. This, theoretically, could result in gains along the axis of the load…parallel to the tensile force.
What is happening along the transverse axis? Physical models for elastic materials would show that the axis parallel to the applied force will shrink. Stay with me - I’ll get back to the grid.
The force stretches the grid and causes the perpendicular lines to get farther apart, while the parallel lines will, in turn, get closer together. Once mitosis begins (and as long as there is NOT significant tissue death) the body will start to “draw” new lines perpendicular to the applied force to reinforce that axis and restore dimensional stability. This is basically understood to be the case and there is plenty of medical literature on the topic. Go ahead and look, you have my blessing.
What is NOT so well understood in what happens to the OTHER axis - the one that gets squished under load. Due to the anecdotal evidence of many good gainers…the penis does not get narrower when stretched or shorter when it is expanded. There are limits, but some expansion is occurring in those dimensions as well.

I wish I understood that better. But what I have come to believe is that length and girth are interdependent and that perhaps Penismith was on to something grand with his “never let it see what’s coming” approach to PE. I am suggesting that the inflammation can be caused by PE work focused on growth in a particular dimension - but perhaps it does not require it to be so. It may sound crazy, but the bee sting trigger is NOT off the table in my personal pursuit for a weightier wang. I am looking at inflammation as a way to usher in the desired chemicals for proliferation and eventual remodelling. It is during proliferation and remodelling that I will apply the necessary force to encourage growth in a specific direction.

I like the idea of expansion in all directions initially. I do not believe this would hinder length gains. In fact, if the penis was girthier, there would be more points on the grid from which to trigger length gains once the applied force was redirected. Just a thought.

I am *swallow hard* also considering a rebuild of my ADS so that I can attempt applying some tensile force to my penis as I sleep. I do not have anything “safe” yet, but I still like the idea for what it represents: Additional hours of applied force during time when my body naturally enters it’s rebuilding phase.

So, in one post, I think I may have sent up at least three red flags and I didn’t have to mention religion even one time. Oh wait…


"Debate the idea..."

Originally Posted by goonbaby
Hmmm. If that turns out to be correct…then YES, that is EXACTLY what I am saying. *cough*

OK

Originally Posted by goonbaby
If my focus was girth gains I might try clamping or heavy jelq, and erect bending routines. There is evidence around here to suggest these methods work, but the mechanism is not well understood - because they do not ALWAYS work and gain can be unpredictable even with a personal history of past successes.

Granted. I was a very easy length gainer. Girth however, if far harder for me to come by.

Originally Posted by goonbaby
Imagine the cellular structure of the phallic tissue could be represented as a grid where each living cell exists at the intersection between two lines. In a relaxed state, the cells are spaced evenly with negligible tensile forces in random directions.

Yep, thats the way I envisaged the “model”

Originally Posted by goonbaby
Once we apply a significant tensile force (of unestablished degree) to the tissues along a single axis we strain the cellular matrix in primarily one direction. Our grid gets distorted in one direction more then the other while under load. The cells sense this and biomechanical triggers will begin the process of reinforcing the tissue to resist the perceived load. What the body meant for good - we meant for evil.

Still with you here.

Originally Posted by goonbaby
The new collagen will be constructed to support the existing matrix, but can it assume the load as long as the load remains constantly applied? Perhaps not. In a sense, the original tissues are still bearing the brunt of the load. If they FAIL, then there is some plastic deformation, and the new tissues will begin to assume loading. This, theoretically, could result in gains along the axis of the load…parallel to the tensile force.


Initially, prior to PE, the collagen is bound together by fairly weak bonds and is orientated in various directions as the tissues of the penis have yet to be subjected to any real axial loading. The higher the loading and the longer we PE, the more orientated the collagen becomes, and the stronger the cross links between the collagen become, and gains begin to slow or stop (due to insufficient loading to overcome the cross links).
This is, in effect, the end of our newbie gains (which not all guys actually experience). OK, here’s where I think the hypothesis starts to skate on thin ice is as much as yes, we have caused remodelling, and yes we have gotten some gains, but we know have a slightly longer dick that is very much stronger than it was before. Ill get back to this in a second.

Originally Posted by goonbaby
What is happening along the transverse axis? Physical models for elastic materials would show that the axis parallel to the applied force will shrink. Stay with me - I’ll get back to the grid.
The force stretches the grid and causes the perpendicular lines to get farther apart, while the parallel lines will, in turn, get closer together. Once mitosis begins (and as long as there is NOT significant tissue death) the body will start to “draw” new lines perpendicular to the applied force to reinforce that axis and restore dimensional stability. This is basically understood to be the case and there is plenty of medical literature on the topic. Go ahead and look, you have my blessing.


OK, so getting back to it, “So, just increase the load” I hear some one say. All well and good, but sooner or later, I think that we build up cross links that are so strong that the force required to break these bonds is higher than the strength of the collagen and we are risking catastrophic failure of the tissues of the penis, which you also seem to allude to above (at least strengthening).
I believe the mechanism is much like work hardening in ferrous alloys due to a “bunch up” of dislocations. Sooner or later, we will create an area of tissue so “brittle” (for lack of a better word) that catastrophic failure is a real possibility.

Originally Posted by goonbaby
What is NOT so well understood in what happens to the OTHER axis - the one that gets squished under load. Due to the anecdotal evidence of many good gainers…the penis does not get narrower when stretched or shorter when it is expanded. There are limits, but some expansion is occurring in those dimensions as well.

Agreed. My dick didn’t get any thinner, just significantly longer. :D

Originally Posted by goonbaby
I wish I understood that better. But what I have come to believe is that length and girth are interdependent and that perhaps Penismith was on to something grand with his “never let it see what’s coming” approach to PE. I am suggesting that the inflammation can be caused by PE work focused on growth in a particular dimension - but perhaps it does not require it to be so. It may sound crazy, but the bee sting trigger is NOT off the table in my personal pursuit for a weightier wang. I am looking at inflammation as a way to usher in the desired chemicals for proliferation and eventual remodelling. It is during proliferation and remodelling that I will apply the necessary force to encourage growth in a specific direction.

I also agree that length and girth are somewhat independent, but am starting to rethink the whole length OR girth focus of peoples routines. Penismith may well have been spot on with that approach.
Sorry, no bee stings for me….ever!

Originally Posted by goonbaby
I am *swallow hard* also considering a rebuild of my ADS so that I can attempt applying some tensile force to my penis as I sleep. I do not have anything “safe” yet, but I still like the idea for what it represents: Additional hours of applied force during time when my body naturally enters it’s rebuilding phase.


Be careful with that idea mate. That risk/reward relationship is stacked very heavily in one direction in my opinion.

Originally Posted by goonbaby
So, in one post, I think I may have sent up at least three red flags and I didn’t have to mention religion even one time. Oh wait…


Thats what its all about isnt it?

I need to do some more research on IPR and then will tackle a girth routine, but with a difference.
Ill will try out my above theory on how the penis should be subjected to “traction” forces depending on the goal.
Ive had a hard time gaining girth, so I have nothing to lose.

Originally Posted by A69
OK, here’s where I think the hypothesis starts to skate on thin ice is as much as yes, we have caused remodelling, and yes we have gotten some gains, but we know have a slightly longer dick that is very much stronger than it was before. …

…”So, just increase the load” I hear some one say. All well and good, but sooner or later, I think that we build up cross links that are so strong that the force required to break these bonds is higher than the strength of the collagen and we are risking catastrophic failure of the tissues of the penis, which you also seem to allude to above (at least strengthening).
I believe the mechanism is much like work hardening in ferrous alloys due to a “bunch up” of dislocations. Sooner or later, we will create an area of tissue so “brittle” (for lack of a better word) that catastrophic failure is a real possibility.


This is where I was when I started thinking about chemical PE and reading up on the stuff Modestoman, Shiver, and even Hobby had to say about it. The natural program the tissue run wants to build up a counter to external forces. I must disable this tendency, but I must do so in a way that will not compromise my health in any significant way.

Relaxin, DMSO, Verapamil…etc. These show some promise for disrupting the “strengthening” of collagen and stimulating reorientation. So, my theory proposes that if gains are slow in the length department…work on girth for a while. When the body starts orienting collagen to resist expansion in that direction - then change directions again. The new collagen bonds will allow for some expansion that you may not have had available before. When the old collagen is gone…the parameters change…and theoretically, your dimensions change.

Originally Posted by A69
Sorry, no bee stings for me….ever!

Be careful with that idea mate. That risk/reward relationship is stacked very heavily in one direction in my opinion.


If I were “careful”, I never would have started PE in the first place. I won’t be stupid about it; I will at least do some reading and experimentation prior to jumping in with both boots. Thanks though.

Originally Posted by A69
I need to do some more research on IPR and then will tackle a girth routine, but with a difference.
Ill will try out my above theory on how the penis should be subjected to “traction” forces depending on the goal.
Ive had a hard time gaining girth, so I have nothing to lose.


Keep us posted here. I am curious and wish you well.


"Debate the idea..."

http://www.mesomorphosis.com/articl…e-tissue-02.htm
“Because ligaments are generally less vascularized than tendons, the healing and repair process takes much longer and, in some ligaments, may regress or disappear completely. Studies demonstrate that remodeled tissue never achieves normal characteristics nor a return to original mechanical properties. Mature repaired ligament tissue lacks the strength of normal ligaments: usually 50-70% of normal tensile strength.”

“Most connective tissue injuries involve damage to the structural components of the tissue. In sports activities, injuries are classified into two types: acute and overuse injuries. Acute traumas occur from lacerations and partial or complete rupture of the tissue. These injuries heal by the repair process described in Part I. Overuse injuries, the most common category, result from chronic overloading or repetitive motion. The capacity of the tissue for repair greatly exceeds degradation and cellular metabolism is altered such that damage occurs at the cellular and structural levels.

Inflammation is the most prominent symptom of both types of injuries. As discussed in Part I, inflammation is a natural part of the healing process in any injury. However, chronic inflammation may lead to increased tissue degradation and impair the repair process. Indeed, chronic inflammation is a major factor in several connective tissue diseases, especially within articular joints. Pharmaceuticals are often used to manage or alleviate symptoms occurring with connective tissue inflammation. However, many of these exogenous substances may alter the healing and repair process.”

YIKES!
Now, would PE qualify as “overuse” or “chronic inflammation”? Me thinks maybe yes?

“Low-intensity exercise is not considered to be injurious to a healthy normal individual. In fact, immobilization can impair normal metabolism and remodeling of connective tissue. When a joint is immobilized, the diminished mechanical loading and unloading of cartilage and surrounding tissues interferes with normal turnover of cells and matrix components. Decreased stimulation of cells results in decreased proteoglycan synthesis. “

Hmmm.

“Many studies demonstrate that collagen production is sensitive to changes in short and long-term food intake. Within 24 hours of fasting of some animal models, collagen synthesis in articular cartilage decreases to 50% of normal. This reduction declines to 8-12% of control levels after 96 hours. Most conditions are not as severe as starvation. However, energy restriction may reduce collagen synthesis depending on duration and degree of food deprivation.”

So, back to my experiment…If I weaken the tissues with Ointment #1 the tissues will be more susceptible to plastic deformation. If I also fast for 24 hours prior to my most strenuous workout…I can increase the amount of controlled damage I cause - without adding force. *gears turning*

“Replacement of tissue pools of macronutrients requires weeks to months and certainly affects turnover rates of tissue components. Likewise, dietary deficiencies or excess and physical activities influence turnover rates.
Calories provide the body with cellular energy for normal metabolism, building and repairing tissues and stimulate hormonal responses.”

“All of the essential AAs are required for synthesis of proteins and other components and growth factors in the extracellular matrix. Some studies show that supplementing certain individual AAs (methionine, lysine, arginine, and proline) to a protein deficient diet may inhibit prolongation of the inflammation phase of connective tissue healing and aid in fiber cross-linking mechanisms during repair.”

…Then when I enter the Proliferation and Remodelling phases I should take LOTS of vitamins, eat a bunch of healthy, good stuff, and let the tissues rebuild their reservoirs of nutrients. Any thoughts?


"Debate the idea..."

GB, keep up the good work, I’m waiting for the final outcome.

Also, you may want to reconsider the lavender oil.

http://www.healthcentral.com/newsdetail/408/533503.html

From this and other articles I’ve read, it mimics estrogen in the body and suppresses testosterone.

I was aware of that possibility with Lavender Oil. Notice that I placed it in Ointment #1.

I am planning on taking advantage of the Testosterone rebound effect. Two of the more controversial chemicals I am considering are DHT for Ointment #2 and IGF-1 R3 for Ointment #3. I didn’t care to include those in my list at the time. I still have not “cleared” them to be included at ANY time. The idea was to spend 21 days softening up the penis and lowering natural test in the hopes that the receptors will increase in sensitivity. Then 21 days of DHT supplementation to trigger some new growth. The last 21 days to recover natural test levels and let the growth hormone proliferate the cells.

All theory…some possibly dangerous. There is always a risk of cancer to contend with when you mess around with biological chemistry…testicular, prostate…I don’t really relish the thought of either.


"Debate the idea..."

Goony, I am impressed with the depth of your analysis. After you figure this all out, I’ve got some wrinkles around my eyes I want you to work on.


Horny Bastard

Originally Posted by mravg
Goony, I am impressed with the depth of your analysis. After you figure this all out, I’ve got some wrinkles around my eyes I want you to work on.


Man, I’ve seen those wrinkles…there is simply nothing science can do for you.

I am so very sorry.


"Debate the idea..."

Seriously, I think your ideas are good and might work, but those are some potent chemicals you are talking about and I personally would be worried about what I am doing to my precious unit. We can’t just visualize our dicks as a collagen rope we need to stretch, it is delicate living tissue, functioning as a result of nerves and blood vessels and complex chemical reactions. What would all those chemicals do to the mylin sheath of your nerves, or the synapses? What about the arterial walls, in terms of structure and function? And the cellular receptors that respond to miniscule changes in localized chemistry?

Nerves fire a little more weakly, arterial endothelium respond more slowly or less veigorously to signals asking them to expand or contract, etc. Damage to endothelium leads to plaque and reduced blood flow. That’s the kind of stuff I would worry about. But I’m just a worrier.

I wish you luck and success (for selfish reasons, because if it all works out I will be following your prescription!) Just be careful and back off if you notice any worrisome signs of trouble!


Horny Bastard

I found this on DMSO.

I was looking at using DMSO for another application, but am now thinking twice about it.

“The major thing (outside of the fact that it is an *extremely* powerful solvent… which can carry any solute directly into the bloodstream) is that on exposure to air it forms a very high and toxic level of peroxides.

Can anyone confirm or deny this?

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