Chemical PE: The Long Awaited Evidence

“Intracavernosal vascular endothelial growth factor (VEGF) injection and adeno-associated virus-mediated VEGF gene therapy prevent and reverse venogenic erectile dysfunction in rats.”

In VEGF-treated rats, regeneration of smooth muscle and nerves as well as endothelial cell hypertrophy and hyperplasia were the prominent features. In our animal model, systemic testosterone replacement or intracavernous VEGF (protein and VEGF gene) prevented the veno-occlusive dysfunction in castrated animals. In rats with established venous leakage, VEGF treatment reversed the cavernosometric findings of leakage. Intracavernous injection of either VEGF protein or VEGF gene may be a preferred therapy to preserve erectile function in patients in whom testosterone therapy is contraindicated.

When citing a source, add a link, to avoid bitching about copyrights.

VGEF could be an alternative to testosterone, still T has wider spectre than VGEF. T doensn’t enlarge penis on healthy subjects. This was spoken already. Can you find a study where VGEF enlarged the penis of healthy subjects? Check if VGEF supplementation can have adverse effects, too.

VEGF can radically increase SM content in animals. It has been proposed as a cure for various forms of ED, but no human trials have yet taken place.

In the study below they injected rats. In four weeks the SM content of the rat penises increased by ~25%.

http://www.scie ncedirect.com/s … 302283804002787

If higher SM content = bigger dick this stuff could be useful. I admit that there is a substantial "IF"
You have been arguing that the tunica is the limiting factor and that more SM does not equal a bigger dick. I have been arguing the opposite.

Big Girtha appears to be one of the most successful clampers. In his posts he repeatedly states that you do not need to be hard when you clamp. I found this hard to understand. I assumed that intracavernosal pressure was the mechanism behind clamping. I could not understand how someone could clamp while soft and get gains. The theory that clamping gains come from a build-up of lymph fluid in the dick explains it.

Check the link.

It is true that T can help maintain VEGF and maintain SM.

To prove me wrong you would have to show that T can either radically increase SM or radically increase VEGF.

http://www.scie ncedirect.com/s … 302283804002787

I know it doesn’t make sense really, but I feel I know what BG was talking about when he talked about being expanded without being hard, and it’s having high intracavernosal pressure yet not being erect. As I say, I know it does not make sense, but there does seem to be a kind of being “ballooned” or whatever that means expanded yet not hard. I am very confident that what BG was referring to was not lymphatic fluid expansion. Of course, the safest thing would be to hear his opinion on the matter directly. Just wanted to throw in that I do not think BG’s recommendation supports theory of lymphatic fluid being important. There actually are several people around who believe that you should never do girth work hard, I think because it causes involvement of tunica fibers oriented in directions you do not want involved (ie divide and conquer). Can’t think off top of head where to find people talking about this though.

Increase VGEF already shown
marinera - Chemical PE: The Long Awaited Evidence

if VGEF increase SM I proved both. ;)

The problem is those aren’t healthy subjects. Haven’t read the study you just posted yet gimme time.

I can’t see the full text neither the abstract. It is pretty clear just from the title, though, that what it shows is that VGEF can restore SM content - they are speaking of aged subjects. So again, it is about using VGEF when T supplementation is not advisable, since T is the ‘first choice’:

"Androgens play a pivotal role in maintaining penile tissue architecture and erection: a review.
Traish AM.
Source

Department of Biochemistry, Institute for Sexual Medicine, Boston University School of Medicine, Center for Advanced Biomedical Research, 700 Albany St, W607, Boston, MA 02118, USA. atraish@bu.edu
Abstract

Androgens are essential for development, growth, and maintenance of penile structure, and regulate erectile physiology by multiple mechanisms. Here we provide a concise overview of the basic research findings pertaining to androgen modulation of erectile tissue architecture and physiology. A significant body of evidence exists pointing to a critical role of androgens in erectile physiology. Studies in animal models have provided fundamental knowledge on the role of androgens in modulating tissue architecture and cellular, molecular, and physiological mechanisms. Based on data from our laboratory and those reported by others, we believe that androgens play a pivotal role in maintaining the structure and function of the peripheral penile nerve network, the structural integrity of the corpora cavernosa, the tunica albuginea, and the endothelium of the cavernous spaces. Further, androgens play an important role in regulating the differentiation of precursor cells into trabecular smooth muscle. In this review, we will focus our discussion on findings pertaining to the role of androgens in regulating penile tissue architectural elements in modulating penile function. This knowledge has a profound impact on the potential use of androgens in the clinical setting to treat patients with erectile dysfunction."

Androgens play a pivotal role in maintaining penile tissue architecture and erection: a review

But T doesn’t enlarge normal penises.

BTW, despite aging cause loss of SM (so ED at a major or minor degree) penile size doesn’t vary statistically in different ages. What this gives?

“androgen replacement *normalized* the expression of VEGF”

To prove me wrong you would have to show that T significantly *increases* VEGF.

(more T ≠ more dick……. If more T = more VEGF…….. more VEGF ≠ more dick )

Normalizing low VEGF means increasing VEGF. To prove you wrong about what?

T does not increas SM. It only preserves SM

more T ≠ more dick……… (IF) more T = more SM ………….. more SM ≠ more dick……….. Therefore Tunica is the limiting factor

I am not sure about the relationship between aging and penis size. Men of a certain age begin to experience erectile dysfunction. Chronic ED is known to reduce penis size.

There is evidence that VEGF can increase SM content in younger animals. I will do more research on this.

Actually, it’s you that should prove that more SM = more dick. Those rats had their dicks enlarged? It became noticeably bigger? Bigger than young rats?

I am trying to argue two things:

(1) more SM = more dick

(to support my theory that pumping for several hours a day or chronic use of ED drugs can lead to SM growth and that this can lead to gains)

(2) more VGEF = more SM

I agree with you that more T≠ more dick

If you could prove that more T = more SM (1) would be incorrect
If you could prove that more T = more VGEF (2) would be incorrect

Simply showing that T is required to maintain VGEF levels and SM content does not count

Maintaining something is very different to increasing something

I will read that study, other related studies and a similar study about IGF and get back to you with a summary.

I actually believe (or want to believe) that we are on the cusp of discovering something spectacular.