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

Dr. Pezzi's book

Dr. Pezzi's book

A book by Dr. Kevin Pezzi claims to reveal

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how to trigger a "second puberty" of penile growth that also rekindles libido and sexual sensation.


The Science of Sex

Have any of you read his work and can weigh in on its claims?

I know his method. Testing it out very soon. Let you know when I do.

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Originally posted by Cya at 8
I know his method. Testing it out very soon. Let you know when I do.

What is his method?

No copyrighted material however clear paraphrasing is acceptable.

We are all anxiously waiting!!!


Check it out guys, no need to have a big dick if you ain't gonna use it!!

The use of Finasteride to upregulate/sensitize the androgen receptor before treatment with DHT. This is supposed to upregulate the mRNA levels and therefore gene expression. I thought of using 3alpha while on Finasteride to finally put to rest this hormone causing growth shit for good.

The theory is that you are androgen insensitive after puberty and Finasteride rectifies this. Makes more sense than 4ad, thats for sure.

The problem, ofcourse, is that all the AR are sensative to DHT and you might grow the prostate as well. You might also have some hair loss doing it this way.


Last edited by Cya at 8 : 08-28-2003 at .

“Doctors routinely see men in their flaccid state, rarely inquire into their erect size, and almost never discuss if there’s been any change in size. With this in mind, I have a difficult time understanding why physicians feel qualified to make a sweeping generalization that penis size is immutable. They believe that to be true because they heard it from another doctor, who just passed on what he heard from another doctor who also didn’t know the truth because he was just relaying a myth that he’d heard or read from someone similarly uninformed. Is this any way for learned professionals to behave?

Why did your penis shrink? That could result from decreased testosterone and especially dihydrotestosterone (DHT), which is derived from testosterone. DHT is known to be the primary catalyst for penile growth. Physicians are taught in medical school that this is important only before the end of puberty; once the penis develops, it’ll maintain that size forever. I know that is wrong, and it frankly doesn’t make any physiological sense to me. As I discuss in my book, the body continuously rebuilds itself. If your house could do the same thing, it could tear off an old shingle and replace it with a new one. In time, your house would replace all of its shingles, and you’d have a new roof. Your body does a fairly good job of renewing itself until you hit middle age, at which time tissue regeneration begins to sputter. After a few more decades, this process slows even more. Wounds heal more slowly, and muscles take longer to regenerate after exercise.

If the cells and molecules in your body were not broken down, you could live off sugar water. You wouldn’t need protein. But you do require dietary protein and other nutrients because tissue destruction and regeneration constantly occur. This process is more rapid than you might imagine, because your body recycles some of its building blocks. Only a fraction of the recycled material is lost in the urine or feces.

The bottom line is that the vast majority of the molecules in your body weren’t there a year ago. The old ones are gone, and new ones have taken their place. Even bone, which may seem as active as a fossil, is torn down and rebuilt. The penis is no exception. Let’s think about this logically. If DHT is critical for stimulating penile growth (and it is), why would this matter only before the end of puberty? Isn’t there still a receptor for DHT after puberty? Yes, of course. Once DHT binds to the receptor, doesn’t it affect DNA transcription, as it does before puberty ends? Yes, of course. However, physicians who contend that penis size is fixed after puberty would have you believe that it doesn’t matter if your DHT level is zero, or if you have DHT bubbling out your ears. Can you think of any other example in which the level of a hormone is totally immaterial to its target tissue? I can’t. I graduated in the top 1% of my class in medical school, so I am not ignorant about how the body works. Hormones exist for one reason: to influence their target tissues.

In reality, the penis becomes less sensitive to DHT after puberty, but the sensitivity is not zero. Thus, the DHT level can influence penile size, but to a much smaller degree than it could before the end of puberty, when the penis was still very sensitive to DHT. As I mentioned before, I don’t think the DHT level matters after puberty in regard to penis size, I know it. (If any physician or scientist doubts this, put your money where your mouth is. Let’s wager a million dollars. You’ll lose.)

After reading all this, you might think that increasing the DHT level is the way to go. It may help a wee bit, but there is a much better secret that I accidentally discovered. First, starve your body of DHT by taking finasteride or another drug that blocks DHT production. If you take this long enough and then stop it cold turkey, your DHT production will resume. However, your body will now be more sensitive to DHT, and penile cells that once yawned when they encountered DHT will spring to life and grow faster than they did in puberty, when the DHT upsurge was much more gradual. Your penis won’t just be larger, it will be exquisitely sensitive, and sex will feel much better. Your libido will increase to the point that you would be called a nymphomaniac, if you were a woman.

Besides DHT, other factors influence penile size. Genetics obviously matters, but it is pointless to discuss them because this is not under your control. In terms of what you can influence, DHT is the most important factor, but there are others. I won’t reiterate everything I said in my book, but I will briefly mention other things that make a difference: other hormones, hormone transport proteins such as sex hormone binding globulin (SHBG) and albumin, cadmium, zinc, antiandrogens, phytoestrogens, exogenous estrogens, endogenous estrogens, xenoestrogens, obesity, numerous drugs and chemicals, collagen, elastin, and a dozen other factors.”

He also mentions NPE in his book. Atleast to use of a pump.


Last edited by Cya at 8 : 08-28-2003 at .

Okay but....

This sounds very cool, but once you’ve starved yourself of DHT and go off fastineride, how do you keep all the hair on your head from falling out!

Anyone who’s use Rogaine for a time and then quit has probably gone through the rebound effect where you had rapid hair loss after stopping. This somewhat maps to what he’s saying, because the rapid hairloss may come from the increased DHT or sensitivity to it.

Guess that’s the trade off? Bigger dick vs. being bald. Touch choice.

Golarge

Use Rogaine.

I’ve been taking finasteride for a couple of months now. Maybe if I stopped cold turkey for a month or two to see what happens… I could restart the finasteride when that’s over. I wonder what would happen to my hair though.

I’ve been on Rogaine for about 8 years, and currently.

Perhaps if this question were asked on a hairloss forum. There are some former finasteride users there who stopped because of side effects.

Finasteride takes a short amount of time to work and a short amount of time to get out of your system. Normal DHT levels may only effect libido and maybe a slight bit of change in penile size. I am going to use a PH that turns into DHT in the blood stream to supplement my own levels while also taking Fin.

I will not do PE while trying this. Though I might give it a shot. Let you guys know what happens.

Cya at 10,
Wouldn’t trying to boost your DHT levels while taking fin defeat the purpose(depriving your body of DHT)?? Don’t you think taking PH while on finasteride might increase Estrogen levels and increase the risk of side effects(gyno, etc..)?

If anything, I would think taking the PH when you go of fin would be the way to go.

This theory is exciting. I wish you much luck!

p.s. Yeah I changed your name :p

I am taking Fin right now and will continue for a few more weeks before adding the PH. The PH I am using converts to DHT without 5ar so I can continue to use finasteride while also using the PH. So many things act as 5ar (the enzyme that converts T to DHT) inhibitors that I dont think Testosterone is the way to go here.

You may be lowering the activity of 5ar without even knowing you are doing so. Even some Essential Fatty Acids can disrupt the activity of 5ar. I am not into watching everything I eat so not to mess with my endogenous DHT level.

I would think some body builders already have taken finasteride ahead of taking dht precursors. In addition, many men stop taking finasteride and I would presume their DHT levels recover - why no reports of an enlarged penis?

Not so. Why would you take DHT with finasteride? Most people take T with Finasteride because the Finasteride blocks the conversion to DHT. Why exactly take a 5ar blocker before DHT? What benifit does DHT have for a body builder?

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In addition, many men stop taking finasteride and I would presume their DHT levels recover - why no reports of an enlarged penis?

In his book, he goes into more about this. Its not like your going to grow an inch. He states that you might grow back what you lost from long term use of Fin. Not many men in the world measure their dick as religously as we do and like I said, Finasteride doesn’t completely stop DHT production and your normal levels as an adult are nowhere close to the levels during puberty. If you stop fin early, more than likely you’ll only see an increase in libido but not so much an increase in size.

We will see how it goes. Oh, do a search on penis size and catration and you’ll see that many men complain of this. Now, if DHT didn’t matter after puberty, why would castration cause shrinkage?

All I am saying is that I want to try this before I actually break down and admit science is right. It this doesn’t work, then I am done with the hormone thing for good. Just makes absolutly no sence for an organ not to be influenced by its target hormone.

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