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Why gains slow!

Originally Posted by Redwood1981
I was reading around a bit, and I’d like to toss this out as a another possible reason why gains slow rather than simply fibrosis.

Slowing Gains Theory
“I have a theory that the quick early gains are due to maximizing the existing tissue
and further gains must be from actual stretching and hyperplasia or hypertrophy of the tissues.
This is a slower process and would require a very disciplined routine to force.”~NotEnough

I think there could be some rearranging that takes place in the beginning. I am not sure if rearranging can account for the length and girth increases some guys get though in their newbie gains. I think it is worth thinking about.

Collagen thermodynamics

I am too tired to figure this out tonight, but I am asking Bib’s age old PE question with pharmacology in mind.

If we can damage collagen with head, stress and or pharmacology, do we want a lot of Vit C around to repair in the extended state?

I am thinking we first do a serious collagen reduction/(de-fib). Then do a newbie routine with a lot of heat during the first half of the routine (Bib). When we do this newbie routine again, what do we want to have around?

Originally Posted by penismith
I am too tired to figure this out tonight, but I am asking Bib’s age old PE question with pharmacology in mind.

If we can damage collagen with head, stress and or pharmacology, do we want a lot of Vit C around to repair in the extended state?

I am thinking we first do a serious collagen reduction/(de-fib). Then do a newbie routine with a lot of heat during the first half of the routine (Bib). When we do this newbie routine again, what do we want to have around?

I meant damage collagen with heat, not head.

Do we break down collagen for a few months to try to bring ourselves back to newbie levels? Do we then add Vit C transdermally while in the extended (hanging or wearing ads) while applying a lot a heat, then let is cool in the extended state? What are the pharmacokinetics of Vit C? What is its temperature stability? Do we want to avoid Vit C like Bib? It seems like we can coordinate our daily supplementation with heat and exercise. What is the rate of collagen synthesis? …

Penismith,

Is the massage you are trying based on Rolfing? I saw from Modesto’s posts that maximum peizoelectric levels were attained with an attack angle of 45 degrees. Also I posted somewhere (pumping forum I think) that when I first started Bromelain I notinced that my flaccid look took on an untrained and very retractable appearance. Not good for flaccid hang but something I would consider conducive to eventual remodelling. I also noticed that this flaccid was easily re-attainable with only a very few PE sessions, which suggests that this can occur far faster than maybe we give it credit for.

Originally Posted by Redwood1981
I was reading around a bit, and I’d like to toss this out as a another possible reason why gains slow rather than simply fibrosis.

Slowing Gains Theory
“I have a theory that the quick early gains are due to maximizing the existing tissue
and further gains must be from actual stretching and hyperplasia or hypertrophy of the tissues.
This is a slower process and would require a very disciplined routine to force.”~NotEnough

It’s my humble opinion that a large proportion (50%+ absolute minimum) of newbie gains are deformation rather than new cell growth. Any newbie who wants up to 1/2” within 1 week should read up on the Infrared stretching posts which document this pretty well. The rapid halt in gains after a week would be very difficult to explain any other way (unless anyone has another angle?).

Originally Posted by Shiver

It’s my humble opinion that a large proportion (50%+ absolute minimum) of newbie gains are deformation rather than new cell growth. Any newbie who wants up to 1/2” within 1 week should read up on the Infrared stretching posts which document this pretty well. The rapid halt in gains after a week would be very difficult to explain any other way (unless anyone has another angle?).

I’d agree with this, at least this is what I believe happened to me.

Question is, is this deformation actual deformation in that are we breaking cross linked bonds or are we simply straightening “crimped” fibers?

It may well be that we are breaking weakly cross linked bonds (initially) and that gains slow due to an increase of the cross links between fibers requiring far greater force to break.

Also, this cross linking may explain why some guys have a spurt of gains following a deconditioning break as during the break, the body has removed the cross links which were no longer required (during the break).

I’d say it is the same thing as learning to stretch and touch your toes. I also suspect that the delta of a penis unstreched or with deformation is the zone that people refer to as cementing. Tissue remodels over time so if it is persistantly being stretched it seems likely that it would eventually become permanent in as much as anything about the body can be described as permanent. And yes, I’d expect that some crosslinking is likely a part of the process.

Originally Posted by Shiver
Penismith,

Is the massage you are trying based on Rolfing? I saw from Modesto’s posts that maximum peizoelectric levels were attained with an attack angle of 45 degrees. Also I posted somewhere (pumping forum I think) that when I first started Bromelain I notinced that my flaccid look took on an untrained and very retractable appearance. Not good for flaccid hang but something I would consider conducive to eventual remodelling. I also noticed that this flaccid was easily re-attainable with only a very few PE sessions, which suggests that this can occur far faster than maybe we give it credit for.

Well, I was sort of thinking in an uneducated sort of way that if any particles of fibrosis are coming loose that I might help the process along by massaging. It sounds a little silly but it is the honest answer.

Yes, I know from my uli work that my penis also adapts very rapidly to exercises. After a few sessions, I hardly get any edema. When I first stared doing pe (back when dinosaurs roamed the earth), it took me many many sessions before edema was not a major problem.

Originally Posted by Shiver
It’s my humble opinion that a large proportion (50%+ absolute minimum) of newbie gains are deformation rather than new cell growth. Any newbie who wants up to 1/2” within 1 week should read up on the Infrared stretching posts which document this pretty well. The rapid halt in gains after a week would be very difficult to explain any other way (unless anyone has another angle?).

It defiantly deserves more thought in that we want to know why gains slow. I have not focused on it too much because it is, from what I understand, a one shot deal. It happened for me once and it will not happen again, if the theory is indeed correct. I think we can reduce the amount of collagen or fibrosis (depending on if you think it is a factor) in a safe way that will allow us to get gains. The big gainers have not just run into one plateau but many, that is, it gets progressively harder in perhaps a step wise or exponential fashion. We can’t do anything about initial tissue remodeling, but we do something about structural reinforcement.

Originally Posted by Shiver
Penismith,

Is the massage you are trying based on Rolfing? I saw from Modesto’s posts that maximum peizoelectric levels were attained with an attack angle of 45 degrees. Also I posted somewhere (pumping forum I think) that when I first started Bromelain I notinced that my flaccid look took on an untrained and very retractable appearance. Not good for flaccid hang but something I would consider conducive to eventual remodelling. I also noticed that this flaccid was easily re-attainable with only a very few PE sessions, which suggests that this can occur far faster than maybe we give it credit for.

I have a lot of reading to do.

This is really good:

Consensus: vitamin C?

Originally Posted by penismith
I think there could be some rearranging that takes place in the beginning. I am not sure if rearranging can account for the length and girth increases some guys get though in their newbie gains. I think it is worth thinking about.

Connective tissues are “visco-elastic,” meaning that they continue to lengthen (creep) under a constant applied force for a period of time. Newbie gains may be nothing more than taking up the visco-elastic slack.

Originally Posted by penismith
Well, I was sort of thinking in an uneducated sort of way that if any particles of fibrosis are coming loose that I might help the process along by massaging. It sounds a little silly but it is the honest answer.

Yes, I know from my uli work that my penis also adapts very rapidly to exercises. After a few sessions, I hardly get any edema. When I first stared doing pe (back when dinosaurs roamed the earth), it took me many many sessions before edema was not a major problem.

I read somewhere that message converts connective tissue “ground substance” from a gel to more or a liquid. Any structural strength that the ground substance provides would tend to be reduced by message. Sounds like a good idea to me.

Originally Posted by ModestoMan
Connective tissues are “visco-elastic,” meaning that they continue to lengthen (creep) under a constant applied force for a period of time. Newbie gains may be nothing more than taking up the visco-elastic slack.

Alright, this seems to be the current topic. Lets find all we can to both build the theory up and tear in down in terms of PE. Lets think about the volume increase newbie gains make and how much one could reasonably gain through tissue remodeling. Lets also look at the internal structures independently to determine what their likely limits are in terms of rearrangement.

We can start with collagen. what sort of % increase in length can take place before it snaps?

Shiver brought up a strong point, being the rate at which some newbie gains are made.

Then I propose we get really quantitative about tissue remodeling. I am envisioning a heating pad with a thermometer. I am hoping to find connective tissue melting point curves and what not.

Then we can incorporate the pharmacology we are learning with the thermodynamics we will learn to put together a routine that makes gaining far easier.

We have an article around here somewhere that covers the temperatures. From memory I think the 42-45 degrees celsius was for deformation, and around 60+ degrees caused significant and progressive denaturing of proteins and shrinkage. The Infrared pad I used (thermotex) has thermal cutouts to keep the temperature within the former range.

On collagen extensibility, again I’m pretty sure that we have documents for that too. I remember seeing an exponential stress/strain curve showing ultimate load failure. I’m having trouble locating it right now, but something like 8%-10% length increase rings a bell before failure.

Deviating slightly, I found this article which might be worth exploring further at some point (about scar contraction) :
http://www.babonline.org/bab/036/0247/0360247.pdf

“In summary, CL313A, an 89% deacetylated chitosan,
inhibited the fibroblast-mediated contraction of collagen
lattices while chitin-50A, a 37% deacetylated chitin sample,
had no effect on contraction. Therefore the deacetylation
level of the chitosan appears to be important for its biological
activity. However, this activity was not universal for all
human dermal fibroblasts cultures tested. Fibroblasts that
had previously been defined as responsive to CL313A in a
proliferation assay were consistently inhibited from contracting
the collagen lattice, whereas those that were
identified as non-responsive showed no effect with treatment
of chitosan. These results further strengthen indications
that highly deacetylated chitosans are more biologically
active than chitin and less deacetylated chitosans
and that highly deacetylated chitosans may be useful as
potential anti-scarring agents and wound-healing therapies.”

While searching for something that addresses the tunica’s response to actual exercise, like PE, I stumbled across yet another decent article on PD. This one lists several treatments, and the reasons for their effectiveness. Some of this is old news, some is new. Colchicine sounds like a promising substance. Note that it’s an anti-inflammatory. I wonder if this works any better (for PE or overconditionaing) than taking Advil every day?

http://www.urologyhealth.org/adult/…cat=11&topic=50

Quote
Conservative approaches: Instead of requiring invasive diagnostic procedures or treatments, men who experience only small plaques, minimal penile curvature and no pain or sexual limitations, need only be reassured that the condition will not lead to malignancy or another chronic disease. Pharmaceutical agents have shown promise for early-stage disease but there are drawbacks. Because of a lack of controlled studies, scientists have yet to establish their true effectiveness. For instance:

Oral vitamin E: It remains a popular treatment for early-stage disease because of its mild side effects and low cost. While uncontrolled studies as far back as 1948 demonstrated decreases in penile curvature and plaque size, investigation continues concerning its effectiveness.

Potassium aminobenzoate: Recent controlled studies have shown that this B-complex substance popular in Central Europe yields some benefits. But it is somewhat expensive, requiring 24 pills each day for three to six months. It is also often associated with gastrointestinal issues, making compliance low.

Tamoxifen: This non-steroidal, antiestrogen medication has been used in the treatment of desmoid tumors, a condition with properties similar to Peyronie’s disease. Researchers claim that inflammation and the production of scar tissue are inhibited. But early-stage disease studies in England have found only marginal improvement with tamoxifen. Like other research in this area, however, these studies include few patients, and no controls, objective improvement measures or long-term follow up.

Colchicine: Another anti-inflammatory agent that decreases collagen development, colchicine has been shown to be slightly beneficial in a few small, uncontrolled studies. Unfortunately, up to 50 percent of patients develop gastrointestinal upset and must discontinue the drug early in treatment.

Injections: Injecting a drug directly into the penile plaque is an attractive alternative to oral medications, which do not specifically target the lesion, or invasive surgical procedures, which carry the inherent risks of general anesthesia, bleeding and infection. Intralesional injection therapies introduce drugs directly into the plaque with a small needle after appropriate anesthesia. Because they offer a minimally invasive approach, these options are popular among men with either early phase disease or who are reluctant to have surgery. Yet their effectiveness is also under investigation. For instance:

Verapamil: Early uncontrolled studies demonstrated that this substance interferes with calcium, a factor shown by in vitro cattle connective tissue cell studies to support collagen transport. As such, intralesional verapamil reduced penile pain and curvature while improving sexual function. Other studies have concluded that it is a reasonable treatment in men with non-calcified plaques and penile angles of less than 30 degrees.
Interferon: The use of these naturally-occurring antiviral, antiproliferative and anti-tumorigenic glycoproteins to treat Peyronie’s disease was born out of experiments demonstrating the antifibrotic effect on skin cells of two different disorders — keloids, overgrowth of collagenous scar tissue and scleroderma, a rare autoimmune disease affecting the body’s connective tissue. In addition to inhibiting proliferation of fibroblast cells, interferons, such as alpha-2b, also stimulate collagenase, which breaks down collagen and scar tissue. Several uncontrolled studies have demonstrated intralesional interferon’s effectiveness in reducing penile pain, curvature and plaque size while improving some sexual function. A current multi-institutional, placebo-controlled trial will hopefully answer many of the questions about intralesional therapy in the near future.

Other investigative therapies: The medical literature is replete with reports on less invasive methods for treating Peyronie’s disease. But the effectiveness of treatments such as high-intensity focused ultrasound and radiation therapy, topical verapamil and iontophoresis, introducing soluble salt ions into the tissue via electric current, must still be investigated before these alternative therapies are considered clinically useful. Likewise, controlled studies using larger patient groups with longer follow ups are necessary to prove that the same high-energy shock waves used to break up kidney stones will have positive effects on Peyronie’s disease.

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