This idea of penis enhancement, and guys posting their "gains" in various forums bothers the scientist in me. It`s not that I always accept the current dogma in any given field of biology-medicine, rather I like to let the data speak for itself, (which is often at odds with the consensus, for various reasons.) and in this case it`s quite clear; Erect penis length cannot currently be altered after reaching adulthood. (Flaccid length might be possible, but not erect.) I`m not trying to be negative here, just realistic. Mechanical means can`t alter erect penis size or circumference, you would have to do it via cellular mechanisms.
The onset of puberty and secondary sexual characteristics are associated with an increase in steroid hormones. In men specifically it`s testosterone (T) and dihydrotestosterone (DHT) that is responsible for the various alterations of the male physique. the increases in T triggers an upregulation of AR proteins in the corpus cavernosa penile tissue. This in turn promotes an increase in transcription of a gene called Keratin 33b, which will yield the effect of penile growth.
https://www.ncbi.nlm.nih.gov/pubmed/24994782
Testosterone by itself, without the androgen receptor upregulation has little to no effect on penis size. That`s the reason micropenis hormone treatment, pre and peri-pubertal, has only a limited effect. It`s also why post-pubertal hormone levels, which are high enough for continued penile growth, do not cause "perpetual" penile growth. (Which I guess is a good thing.)
What causes the penis to stop growing seems to be mainly a downregulation of the AR receptor. (As measured by mRNA in the corpus cavernosa.) This is coupled with an increase in a cytokine called TGF-b, that seems to serve as a molecular "break" on penis growth, together with the reduced AR levels again. Neither androgens nor TGF-b can downregulate AR receptor levels. https://www.ncbi.nlm.nih.gov/pubmed/8639466
This is really the question that needs to be answered;
...to the factors responsible for penile AR down-regulation during sexual maturation, because neither androgens nor TGF-b can decrease penile AR protein concentration in immature rats. Our current experiments demonstrate conclusively that the reduction of androgen binding and AR mRNA with sexual maturation is indeed a down-regulation of AR protein and not a binding artifact or an mRNA processing not affecting the steady state levels of the AR protein. This agrees with immunocytochemical observations. The conservation of basal levels of ARs in the adult rat penis that has practically ceased to enlarge is probably due to the need to maintain some degree of androgen responsiveness unrelated to growth, such as nitric oxide-dependent penile erection…
https://onlinelibrary.wiley.com/doi/pdf/....tb02469.x
So you need to find a way of increasing the transcription of either AR protein, specific for penile tissue, or transcription of the downstream keratin 33b gene. (Maybe a better way.) The way to do this would be AAV gene therapy. I actually think this would work currently in a rat model and could be done without major difficulties. You could also then study potential side effects like cancer. Cancer is an issue when you`re dealing with cell proliferation/growth. But if you where successful here you could then move to human clinical trials, maybe men with micropenis first.
There is a way to progress here for someone who is invested enough to actually do something about this. (It`s not important enough for me, although I`d take an extra inch if it becomes available.) Trying to crowdfund a study like I mentioned in a rat model with gene therapy would be a way to do it. If you can prove it works in an animal model you would have headline news, and probably the rest would solve itself. (funding etc.) The market for a treatment is definitely there. Makes a lot more sense than wasting your time hanging weight`s from your dick. (In my opinion.)
The onset of puberty and secondary sexual characteristics are associated with an increase in steroid hormones. In men specifically it`s testosterone (T) and dihydrotestosterone (DHT) that is responsible for the various alterations of the male physique. the increases in T triggers an upregulation of AR proteins in the corpus cavernosa penile tissue. This in turn promotes an increase in transcription of a gene called Keratin 33b, which will yield the effect of penile growth.
https://www.ncbi.nlm.nih.gov/pubmed/24994782
Testosterone by itself, without the androgen receptor upregulation has little to no effect on penis size. That`s the reason micropenis hormone treatment, pre and peri-pubertal, has only a limited effect. It`s also why post-pubertal hormone levels, which are high enough for continued penile growth, do not cause "perpetual" penile growth. (Which I guess is a good thing.)
What causes the penis to stop growing seems to be mainly a downregulation of the AR receptor. (As measured by mRNA in the corpus cavernosa.) This is coupled with an increase in a cytokine called TGF-b, that seems to serve as a molecular "break" on penis growth, together with the reduced AR levels again. Neither androgens nor TGF-b can downregulate AR receptor levels. https://www.ncbi.nlm.nih.gov/pubmed/8639466
This is really the question that needs to be answered;
...to the factors responsible for penile AR down-regulation during sexual maturation, because neither androgens nor TGF-b can decrease penile AR protein concentration in immature rats. Our current experiments demonstrate conclusively that the reduction of androgen binding and AR mRNA with sexual maturation is indeed a down-regulation of AR protein and not a binding artifact or an mRNA processing not affecting the steady state levels of the AR protein. This agrees with immunocytochemical observations. The conservation of basal levels of ARs in the adult rat penis that has practically ceased to enlarge is probably due to the need to maintain some degree of androgen responsiveness unrelated to growth, such as nitric oxide-dependent penile erection…
https://onlinelibrary.wiley.com/doi/pdf/....tb02469.x
So you need to find a way of increasing the transcription of either AR protein, specific for penile tissue, or transcription of the downstream keratin 33b gene. (Maybe a better way.) The way to do this would be AAV gene therapy. I actually think this would work currently in a rat model and could be done without major difficulties. You could also then study potential side effects like cancer. Cancer is an issue when you`re dealing with cell proliferation/growth. But if you where successful here you could then move to human clinical trials, maybe men with micropenis first.
There is a way to progress here for someone who is invested enough to actually do something about this. (It`s not important enough for me, although I`d take an extra inch if it becomes available.) Trying to crowdfund a study like I mentioned in a rat model with gene therapy would be a way to do it. If you can prove it works in an animal model you would have headline news, and probably the rest would solve itself. (funding etc.) The market for a treatment is definitely there. Makes a lot more sense than wasting your time hanging weight`s from your dick. (In my opinion.)
We will stomp to the top with the wind in our teeth.
George L. Mallory