Penis Enlargement Guide
There are a total of three analyses on this issue in the literature. Fraiman et al. studied 100 men less than six months after radical prostatectomy, and took preoperative and postoperative flaccid and erect measurements and demonstrated an overall mean reduction in erect penile length of 9 but a mean reduction in volume of 22 1 . Munding et al. studied 31 men and measured penile length in the stretched flaccid state (accepted as equivalent to erect length) and showed that 71 had a decrease in penile length compared to preoperatively, with 48 of men demonstrating greater than a 1 cm loss and a range of loss of 0.5-4cm 2 . Finally, Savoie et al. studied 63 patients with preoperative measurements followed by repeat measurement, at three months postopera-tively, and demonstrated that 68 of patients had some degree of length loss. The authors also showed that in this population there was no difference between patients with erectile dysfunction (ED) and those without, postoperatively 3 ....
3 Penile length One of the primary concerns of patients preopera-tively is penile length loss. At presentation many men complain of loss of penile length, and by the time many patients have reached comfort level with surgical intervention most have already experienced this problem. Thus, any further loss of length is a major concern. In patients with penile curvature, an assessment at full rigidity of penile length on the concave and convex sides may give a crude estimate of the potential for length loss if plication-type procedures are employed. Furthermore, having penile length documented preoperatively permits comparison to postoperative length in men who complain of postoperative length loss. Most authorities agree that an assessment of erectile hemodynamics
Following discharge from hospital, the patient should be followed-up within a few weeks for wound assessment. At further follow-up meetings, assessment of residual erectile function should be made. While postulated, the role of strategies for penile fibrosis minimization (oral colchicine) and penile length preservation (vacuum device) is unclear in the absence of outcomes data. Any conversation with the patient regarding the use of erectogenic medications (phosphodiesterase-5 (PDE-5) inhibitors, intra-urethral agents, intracavernosal injection agents) must include discussing the fact that men with a history of priapism using such agents must be carefully monitored. Patients using erecto-genic medications must be monitored closely. While intriguing, the animal data supporting reduction in priapism events in sickle cell mice with chronic PDE-5 inhibitor administration is preliminary and no human studies have been conducted to date.
If mechanical problems in an inflatable device develop after surgery, a trend to remove and replace the entire device has emerged recently. Common mechanical failures are tubing fracture, cylinder or reservoir leak, cylinder aneurysm, or connector disruption. Most urologists consider that replacing the entire device will give the patient added longevity in all parts 14,30 . Certainly after two or three years, it is prudent to replace all the prosthesis components because there can be significant wear of the device within that period. In addition, repeated penile incisions to change cylinders may shorten the penile length 34 . Furthermore, bacteria-positive cultures of clinically uninfected penile prostheses have been found in 70 of tested implants. In some patients, more than one organism grew, and in some patients the pump culture was negative but the biofilm was positive 35 . This may explain the higher infection rate that occurs with revision surgery 36,37,38 . Combining complete...
While there may be skepticism about the validity of human sperm competition theories, experimental research takes these theories quite seriously. Presuming that human sperm competition exists, studies have been designed to explore the role of human sperm competition in the context of male anatomy, male psychology and behavior, and human reproduction. One such study hypothesized that the human penis may have evolved as a semen displacement device.54 A research team created artificial anatomical models of male genitalia complete with simulated semen to test the hypothesis that the human penis is designed to displace semen deposited by other men in the reproductive tract of a woman (figure 2.3). Figure 2.4. The semen is displaced by one of the phalluses with a coronal ridge after the experiment. From G. G. Gallup, R. L. Burch, M. L. Zappieri, R. A. Parvez, M. L. Stockwell, and J. A. Davis, The Human Penis as a Semen Displacement Device, in Evolution and Human Behavior 24 (2003) 277-289....
Most recently, Choi et al. at Memorial Sloan Kettering Cancer Center analyzed 392 patients for this problem 24 . Fourteen percent (47 392) reported orgasm-associated urine leak (OAI). No difference in OAI rates were noted based on nervesparing or type of radical pelvic surgery. Men reporting OAI were more likely to complain of penile length loss (44 ) than men not reporting OAI (26 , P 0.01). Likewise, they were more likely to report orgasm pain (18.5 ) compared to men without OAI (2 , p 0.01). On multivariate analysis, both factors remained predictive reporting penile length loss, OR 2.25, P 0.01 orgasm pain, OR 10.42, P 0.01.
Various surgical techniques have been developed to restore genital abnormalities, e.g. epispadias, micropenis, penile carcinoma, genital trauma, corporal fibrosis, and Peyronie's disease. In many of these cases there is a limited amount of cavernosal tissue and surgeons have relied on prosthetic devices to recover the patient's erectile function 2 .
Development disorders of the internal and external genitals may be caused by chromosomal defects, disorders of testosterone and DHT synthesis, or disorders of androgen receptor functions (androgen resistance) and the Mullerian inhibiting hormone. Thus synchronous, combined action of testosterone, DHT and Mullerian inhibiting factor is essential for normal development of the internal and external genitals. In this regard fetal and pu-bertal development of the penis length first and foremost depends on sufficient testosterone and DHT tissue levels and, second, by the number of androgen receptors 3-5 .
The clinical picture of androgen deficiency is dependent on the age at which this deficiency appears, and on its extent 1 . Prenatally, depending on the phase of development, it may result in intersexuality, or in abnormal positioning of the testes and an abnormally small penis (micropenis). Congenital penile deviations may also be the result of a temporary T deficiency or androgen insensitivity during fetal development 17 . Between birth and puberty
If advances in penile enlargement surgery become possible in the future, they should be translated to penile implant surgery 24 . A similar problem has to be solved for patients with severe Peyronie's disease, who require incision or resection of their plaques during the implant surgery. The ideal graft material to cover defects in the tunica has yet to be found. It should have tensile strength and stretching characteristics similar to those of healthy tunica albuginea. Future advances should also include tissue welding techniques to replace time-consuming suturing 24 .
It has been proven that GH and IGF-1 affect penis growth and androgen production 54 . In cases with isolated GH deficiency and micropenis, continuous treatment with recombinant growth hormone normalizes the penile size 54 . Recently it has been suggested that GH also plays a role in erection 55 . Recombinant GH caused dose-dependent relaxation of cavernous smooth musculature by increasing intracellular cGMP levels. During erection a 90 increase in intracavernous GH concentration occurred in the tumescence stage.
For a few years in the early 1990s, I worked on a national sex information switchboard. Much to my surprise, a majority of the callers were men, and their two most common questions were What is the normal penis size and Where is the clitoris Trained to provide anonymous, nonjudgmental, and accurate information to callers, I would respond that most penises, when erect, were between 5 and 7 inches. I would receive immediate thanks for this information, and as they hung up I remember thinking their relief was palpable. Their penises, presumably, were okay.
It is difficult to distinguish the signs and symptoms of androgen deficiency from GH deficiency as they are quite similar 168 . Both androgens and GH decrease with age, making evaluation of cause and effect difficult if the cause may be due to a pituitary problem. Also, GH replacement reverses the same symptoms as does T-replacement 335 . The biologic effects of GH and androgens are mutually interdependent and synergistic 336 . But in boys with micropenis and GH and T defiiciency, treatment with GH alone resulted in a normal penis size 337 . Most biologic effects of GH are not mediated by itself but by insulinlike growth factor (IGF)-1 which is synthesized in the liver cells following stimulation by GH, or locally in target tissues of GH, and is released into the bloodstream from there.
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