Gain .5 inch/month with no excersizes

Sorry man, I’m missing your point.

Would what still be the case? What exactly are you questioning in regard to test / DHT?

I really think this is by FAR the most important aspect of the entire process. Now the question really is:

Which 3 HSD enzyme is more prominant in the penis???

This is of utmost importance, if using a PH or steriodal component as the active.

Thoughts??

Would DHT be considered both androgenic and anobolic if it wasnt deactivated?

Could Large quantities of T simulate the effect of DHT?
Is there a local 5ar enyme in the penis?

And here is the only info I’ve been able to dig up on enzyme activity in prostrate/penise.

Acta Endocrinol (Copenh) 1975 Jun;79(2):394-402 Related Articles, Links

In vivo uptake and metabolism of 3-h-5alpha-androstane-3alpha,17beta-diol and of 3-h-5alpha-androstane-3beta,17beta-diol by human prostatic hypertrophy.

Horst HJ, Dennis M, Kaufmann J, Voigt KD.

Tritiated 5alpha-androstane-3alpha,17beta-diol (3alpha-diol) and 5alpha-androstane-3beta,17beta-diol (3beta-diol) respectively were administered to patients with benign prostatic hypertrophy (bph) undergoing prostatectomy. In prostate and skeletal muscle homogenates and in plasma the total radioactivity content as well as the formation of metabolites were measured. Histological examination of each ectomized prostate was performed to evaluate the cellular composition of the tissue. After 3alpha-diol injection, a higher uptake of radioactivity in the prostate was obtained than after 3beta-diol. Within 30 min the 3alpha-isomer was very efficiently converted to 5alpha-DHT, while most of the 3beta-isomer remained unchanged. There was, however, also after administration of the 3beta-diol a substantial biconversion to 5alpha-DHT as has been confirmed by recrystallization to constant specific radioactivity. Only after 3beta-diol epiandrosterone was detected in small but significant amounts. 3alpha-diol administration resulted in distinct concentrations of 3beta-diol, whereas the conversion of 3beta-diol to the 3alpha-isomer was insignificant. When comparing the histological composition of the prostatic tissue with the accumulation of radioactivity and the formation of metabolites only a weak correlation between glandular structure and radioactivity uptake after 3alpha-diol administration could be revealed.

PMID: 49141 [PubMed - indexed for MEDLINE]

J Endocrinol 1975 Mar;64(3):529-38 Related Articles, Links

Binding and metabolism of 5alpha-androstane-3alpha, 17 beta-diol and of 5alpha-androstane-3beta, 17 beta-diol in the prostate, seminal vesicles and plasma of male rats: studies in vivo and in vitro.

Krieg M, Horst HJ, Sterba ML.

Binding of 5alpha-androstane-3alpha, 17 beta-diol (3alpha-diol) and 5alpha-androstane-3beta,-17 beta-diol (3beta-diol) in vivo and in vitro to the 100 000 g cytosol fraction of the rat prostate and seminal vesicles as well as to plasma was studied by agargel electrophoresis and sucrose density gradient ultracentrifugation and the results compared with the corresponding findings for 5alpha-dihydrotestosterone (5alpha-DHT). The metabolism of 3alpha-diol and 3beta-diol was also investigated by thin-layer chromatography. The following results were obtained: (1) A specific binding of 3alpha-diol and 3beta-diol by the cytosols could not be demonstrated in vitro, while 5alpha-DHT was specifically bound. (2) In plasma, 3alpha-diol was extensively bound, 3beta-diol less extensively bound, while 5alpha-DHT remained unbound. (3) After intravenous injection of 3alpha-diol, specifically bound radioactivity, increasing within 30 min, was found in the prostate cytosol, while after 3beta-diol injection no binding occurred. (4) Parallel to the increased binding, the total radioactivity in the prostate accumulated within 30 min after 3alpha-diol injection, the uptake being 5-3 times higher than in skeletal muscle. However after 3beta-diol injection, total radioactivity decreased in the prostate within 30 min, the uptake being only 1-5 times higher than in skeletal muscle. (5) One minute after injection of 3alpha-diol, 53% of the extracted radioactivity in the prostate had been converted to 5alpha-DHT, this increased within 30 min to 81%. Thirty minutes after the injection of 3beta-diol, about 32% of the extracted radioactivity in the prostate had been converted to 5alpha-DHT. (6) From the in-vivo and in-vitro experiments it was concluded that 3alpha-diol exerts its biological effects mainly by its conversion into 5alpha-DHT.

PMID: 1133541 [PubMed - indexed for MEDLINE]

Check out those conversion rates! I’m not sure what the carryover is between the seminal vesicles of a rat compared to humans is, but I thought it was interesting.

Oh,

NO. Absolutely not.

They have two completely different methods of action.

Large quantities of t would still not have the same androgenic characteristics of DHT (facial hair growth, deepening of the voice, etc…)

DHT doesn’t poses the power to stimulate skeletal muscle growth.

Two very different actives.

Anyway,

Based on the studies posted above, if we accept that rat nuts respond in likeness to human corpus cavernosum as fact, and I’m not saying that it is…..

What active does that tell us we should be using?

Thoughts?

Yes, 3-alpha converts to DHT via the 3 HSD enyme at a 40% clip. So, in theory, if you use a local carrier plus 3alpha then you have a much more effective product. I did say product didnt I?

Bro,

More info on this significant differance.

DHT:
DHT is the conversion product of testosterone at the 5-alpha-reductase enzyme, the result being a hormone that is 3 to 4 times as androgenic and is structurally incapable of forming estrogen.

One would imagine then that DHT would be a perfect drug to enhance strength and add small but completely lean gains to the frame. Unfortunately there is a control mechanism for DHT in the human body. When levels get too high, the 3alpha hydroxysteroid dehydrogenase enzyme converts it to a mostly inactive compound known as 3-alpha (5-alpha-androstan-3alpha,17beta-diol), a prohormone if you will. It can equally convert back to DHT by way of the same enzyme when low levels of DHT are detected. But it means that most of what is administered is quite useless at the height of the androgen receptor in muscle tissue and thus DHT is not particularly suited, if at all, to promote muscle hypertrophy.

Testosterone:
Testosterone is the prime male androgen in the body, and as such still the best possible mass builder in the world. It has a high risk of side-effects because it readily converts and forms estrogen quite easily. But these characteristics also provide it with its extreme anabolic tendencies. On the one hand estrogen increases growth hormone output, glucose utilization, improves immunity and upgrades the androgen receptor, while on the other hand testosterone is extremely potent at activating the androgen receptor and eliciting major strength and size gains.

Well, well, well…

Someone is actually paying attention.

So….why are we still using 4AD a known testosterone precursor and not 3-alpha a known DHT precursor?

Just a thought kids…

Topical DHT 2.5% 1.7ml qd, Androgel 1% 5g qd. He knows our wishes
to conceive.

NOW!

Before everyone starts rubbing 3-alpha on their dick…let’s think about this.

Our idea here is to introduce androgenic PH’s (not fvcking anabolic…) locally into the penis… the problem as you MAY NOT know is that this tissue runs behind the scrotum down almost to your anus and then right into your prostate, the actuall implications are significant the real danger is unknown. The support for the theory is puberty and perhaps the side effect of PH’s/steroids on the clitoris which is for all intents and purposes the same tissue type. The problem is we don’t really know why the penis stops growing in puberty. Most men reach a full size well before they are done with puberty and even more so before their natural test levels start to decline with age. Point being that constant stimulation does not apear to do it. The receptors might down regulate possibly or perhaps its an androgen shock that causes the growth. GH seams to play a role as well although I’m not sure if its GH dirrectly or IGF-1. if the former then running the experiement on a keto diet might help things. (sorry, that’s a side thought and not all that relavant right now…)

I think it this can be done but NOT by looking at what causes it but WHY! Remember the body’s first concern is supply energy to the brain and then to insure the reproductive organs are working and full speed… this likely has something to do with the latter, the trick would be to find out how to make the body think the penis isn’t long enough to do it’s job and let the body induce growth possibly with some help at that point.

The basic wrap here is that you shouldn’t be rubbing a DHT precursor on your cock if you don’t want prostrate inflamation/serious trouble….

So how do we protect the prostrate AND deliver the DHT??

Don’t know…but that’s some thoughts.

Thanks B&B,

Why was this initially prescribed? HRT?

“Nearlythere,

Thank you for the information.

I won’t say what I want to say, to Jonesy but………”

sunshinekid, what is it you would like to say? The information provided is 100 percent in accord with what I said.

“Dihydrotestosterone binds the androgen receptor much more strongly than does testosterone at the same concentration, yielding a higher degree of ligand-receptor stability. When the concentration of testosterone is increased however, the receptor stability increases to a level similar to that seen with dihydrotestosterone “

When levels of T are increases, the action is similar to DHT. Hmm, thats exactly what I said.

“DHT is not considered anabolic because it is not active in skeletal muscle (it is enzymatically deactivated);”

Again, this shows that DHT can do exactly what testosterone can do. Your post states that the reason why DHT does not strongly bind to muscle cell ARs is because of local enymes convert it into something else. Thanks for posting enough information to show how flawed your conclusion was.

This information was also irrelevant to PE. It was talking about muscle cells and the enzymes which exist there to act upon DHT. We are concerned with that of the penis.

If DHT is altered by enzymes, then yes, it then cannot have the same effect on ARs. That should be common sense.

“So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to say that administering exogenous DHT is not without any anabolic effect. It actually does have some anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone. This is due to its quick breakdown by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If this enzyme were somehow blocked, it is likely that DHT would exhibit very potent anabolic effects on muscle.”

This is another “opinion.”

Bro, test and DHT are different hormones that exhibit different methods of action. Period. End of story. This is basic first year stuff.

Ok.

Post studies other than the ones I already have that cleary show enzyme activity in penile tissue.

I’ll be waiting.