Thunder's Place

The big penis and mens' sexual health source, increasing penis size around the world.

Gain .5 inch/month with no excersizes

I haven’t read all 45 pages of this thread (Sorry!), so if my contribution has already been covered, please accept my apologies.

It is my understanding that the conversion of 4AD and other prohormones to testosterone takes place only in the liver. So what is the point of applying it directly to the penis shaft rather than to other areas of the body where the skin is relatively thin (i.e., the inner thighs and inner arms and, because the skin is relatively thin and well-supplied with blood vessels, the scrotum (but watch out for alcohol-based products)). In all cases, the prohormone has to be transported by the blood stream to the liver, where it is converted to T and then redistributed to T receptors *throughout the body*. That means that no more of the T resulting from the application of a prohormone to the shaft will come back to the shaft than it would if applied to any other part of the body.

The application of Androgel directly to the shaft is another story altogether. It already contains T and therefore does not need to go to the liver for processing and is ready to go to work wherever applied; so, if T will indeed induce penis growth, it is likely that a greater concentration of it will end up in the penis.

Awhile back on a Yahoo forum that no longer exists, the owner-moderator (Ken, are you there?) reported on a theory-hypothesis-supposition that dihydrotestosterone and human growth hormone injected directly into the penis might result in growth, the theory being that the receptors responsible for penis growth might be reawakened by being flooded with the relevant hormones.

A poster on another forum dealing with PE reported on his results from a series of penis surgeries, hanging and, at the direction of his surgeon, injections of either T or hGH (I don’t remember which, and the forum seems to have shut down, at least for the time being). His gains were from about 6” in length to 8” or more and to about 6” in girth.

Any input?

transdermal prohormones don’t go to the liver to be converted into the target hormone that’s the whole reason there topical so they don’t get broken down by the liver like an oral form, and they convert with enzyme’s circulating in the blood. the qusetion is how do you keep the prohorme in one site like the penis with out it go’ing systematic.

I disagree with pumpin4big1. Prohormones taken orally are broken down in the stomach and never make it to the liver; the stomach sees them as just another protein to be digested. The reason for taking prohormones transdermally is to avoid the stomach, but they still must go to the liver to be converted into T. There are no enzymes in the body generally capable of converting prohormones to T.

Supposedly there are two ways to up-regulate the androgen receptors.

Does anyone know?

Is one of them DHT?

Originally posted by chi8wannabe
There are no enzymes in the body generally capable of converting prohormones to T.

This isn’t ‘strictly’ true. 5AR is not confined to the liver. Other organs (including the prostate) have their own supply of the enzume, which is why people are concerned about putting prohormones on their unit, since it is in realatively close proximity to the prostate. Sebaceous glands and hair root cells are other concentrated areas, hence the expression of DHT side effects found there. It is not just free floating DHT that causes these changes, but locally metabolized DHT via the 5AR.

Also, 4AD doesn’t need 5AR since it is active in its own right. If you want the 4AD to convert to Test then that of course would be a different matter.

Originally posted by skeetersonme
Supposedly there are two ways to up-regulate the androgen receptors.

Does anyone know?

Is one of them DHT?

That’s an excellent question, and I wish I had an answer :)

If we could upregulate the AR locally, then there would be no need to add androgen, since systemic levels would suffice.

If you find any evidence supporting AR upregulation via a non androgen axis then I would be very interested indeed!

4ad converts to Test via the 3b-HSD enzyme that can be found all over the body including the penis.

If you find any evidence supporting AR upregulation via a non androgen axis then I would be very interested indeed!

Now this would be a magic bean!

Is 3b or 3a found in the penis? I remember reading something that says 3a is found in the prostate.

They both are found in the penis, just at different levels.

I think a local carrier is key! Maybe this stuff called gel #3. Supposedly it is a local carrier. Someone called “xextreme formulations” is trying to sell it in a product called synstance (spelling is wrong). I think it contains 1,4ad. They are trying to provide local growth of muscles. I emailed them and they said the product will be released at the end of the month. Someone said the FDA got involved, so who knows.

Anyway, I think the main components are local carrier, how to get AR upregulated (DHT?) and maybe 3 alpha has something to do with it. Maybe this is why you have a better chance of success with Androgel.

So maybe real test. and this local carrier (#3) will work. The only thing missing is upregulating the receptors.

Any thoughts!!

I thought this was interesting!!…2&dopt=Abstract

Up-regulation of the levels of androgen receptor and its mRNA by androgens in smooth-muscle cells from rat penis.

Gonzalez-Cadavid N, Vernet D, Fuentes Navarro A, Rodriguez JA, Swerdloff RS, Rajfer J.

Department of Surgery, UCLA School of Medicine, Harbor-UCLA Medical Center, Torrance 90509.

Smooth-muscle cells cultured from the penis of sexually immature (I-PSMC) and adult (A-PSMC) rats express similar high levels of the androgen receptor (AR) mRNA. This contrasts with the marked in vivo decline of both AR mRNA and androgen binding in the penile smooth muscle of adult rats, which appears to be responsible for the cessation of androgen-dependent penile growth upon sexual maturation. PSMC is therefore a good model to study putative down-regulators of AR expression as a function of cell proliferation in the smooth muscle of androgen-responsive vascular tissue. In order to determine whether AR protein levels in PSMC correlate with AR mRNA levels, the immunocytochemical detection of ARs and their androgen binding capacity were compared between I- and A-PSMC. The number of ARs and their protein half-lives suggested similar levels of translation of the AR mRNA in both cell lines. The effect of the synthetic analog methyltrienolone (R-1881) on androgen binding was studied in contact-inhibited androgen-deprived PSMC. In contrast to the postulated role of androgens as down-regulators of AR expression in rat penis, ARs were up-regulated in A-PSMC by R-1881. Contact inhibition of A-PSMC combined with serum depletion and androgen deprivation down-regulated AR mRNA levels, and dihydrotestosterone (DHT) counteracted this effect. These results suggest that the loss in A-PSMC of the age-dependent down-regulation of ARs observed in vivo in adult corpora cavernosa smooth muscle is related to the in vitro resumption of cell proliferation and that DHT acts directly on the penile smooth muscle as a positive modulator of AR levels.

Testosterone down-regulates the levels of androgen receptor mRNA in smooth muscle cells from the rat corpora cavernosa via aromatization to estrogens.

Lin MC, Rajfer J, Swerdloff RS, Gonzalez-Cadavid NF.

Department of Surgery, UCLA School of Medicine, Torrance 90509.

Androgens down-regulate the levels of androgen receptors (AR) and AR mRNA in the penis and prostate of castrated rats, and are assumed to cause their decrease during sexual maturation in the penile smooth muscle of intact rats. In order to determine whether these effects occur directly at the target cell level, and to what extent they are due to testosterone (T) or to their metabolites, we have measured AR mRNA in cultures of smooth muscle cells from the adult rat corpora cavernosa treated in vitro with sex steroids. T at high concentrations (100 nM) acted like dihydrotestosterone (DHT) in increasing moderately the levels of AR mRNA in both proliferating and contact-inhibited cells. However, when conversion of T to DHT was blocked by the 5-alpha reductase inhibitor finasteride, the levels of AR mRNA were considerably down-regulated by T (10-500 nM), particularly in the contact-inhibited cells. Finasteride by itself was inactive. These effects in both types of cultures were inhibited by platelet derived growth factor (PDGF) (20 ng/ml), a growth factor that up-regulates AR mRNA levels, and by fadrozole (100 nM), an aromatase inhibitor of the T/estrogen conversion. Estradiol (50 nM) was even more potent than T in decreasing AR mRNA levels. With the exception of PDGF none of the treatments affected significantly cell growth, as measured by DNA synthesis and content. Our results indicate that it is possible to modulate in vitro AR mRNA levels in the penile smooth muscle cells, and that under normal conditions DHT and T act as moderate up-regulators. When DHT formation is inhibited, the aromatization pathway of T to estradiol will prevail and induce a pronounced down-regulation of AR mRNA levels. We assume that the in vivo AR down-regulation in the penile smooth muscle by androgens is an indirect effect mediated by a paracrine or endocrine mechanism elicited in another tissue.

Yes but how do you want to use DHT and not effect your hair, prostate, acne or body hair? It must be atleast 75% local not to effect other ARs.

#3 is no where close to this level of site specific activity. Also, it contains Benzyl Alcohol. This will, at the very least, burn your sensitive skin.

Harmful if inhaled or swallowed. May be harmful if absorbed through skin.
Eye and skin irritant.”

Ingredients: Isopropyl alcohol, benzyl alcohol, octyl salicylate, triglyceride complex, water, d-limonene, carbomer

You can always inject DHT or use a device to drip it into the urethra but neither of these seem to be appealing to me.


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