epro said:What dosage you suggest?
http://www.ncbi.nlm.nih.gov/pubmed/7534702Dihydrotestosterone is the active androgen in the maintenance of nitric oxide-mediated penile erection in the rat.
Abstract
Androgens are essential for the expression of normal libido in the male, but their role in the maintenance of the erectile response in humans is controversial. It has been shown previously in the rat that castration induces 1) loss of penile reflexes; and 2) considerable reduction in the erectile response to electric field stimulation (EFS) of the cavernosal nerve. Both of these effects can be reversed by testosterone replacement. The current study was performed to determine whether these testosterone effects are mediated via its conversion to dihydrotestosterone (DHT), and to what extent the synthesis of the mediator of penile erection, nitric oxide, is affected by castration and androgen replacement. Five-month-old rats were either castrated or left intact. The orchiectomized rats were implanted with SILASTIC brand silicon tubing (Dow Corning) containing testosterone or DHT with or without daily injections of the 5 alpha-reductase inhibitor finasteride. After 7 days, rats were submitted to EFS and the intracavernosal pressure was recorded. Castration reduced the EFS-induced erectile response by 50% in comparison with intact rats and testosterone restored this decrease to normal. When finasteride was given to these testosterone-treated castrate rats, erectile response was not restored. DHT was as effective as testosterone in restoring response to EFS in castrates and this effect was not decreased by finasteride. Nitric oxide synthase activity in the penile cytosol was measured by the arginine-citrulline conversion and was found to correlate with the EFS determinations. These results show that DHT is the active androgen in the prevention of erectile failure seen in castrated rats, and suggest that this effect may be mediated, at least partially, by changes in nitric oxide synthase levels in the penis.
http://www.sexualmed.org/index.cfm/risk ... d-avodart/Irwin Goldstein
The pathophysiology of 5 alpha reductase inhibitors on sexual function may be related to reduction of dihydrotestosterone levels. Nitric oxide and the enzyme, nitric oxide synthase are critically important in sexually stimulated penile erections. Dihydrotestosterone is more potent than testosterone in raising nitric oxide synthase activity. Because 5 alpha reductase inhibitors reduce serum levels of dihydrotestosterone, this effect may be responsible for erectile dysfunction by reducing levels of nitric oxide and reducing nitric oxide synthase activity in the penile erection tissues
Researchers have documented that at high doses, finasteride impaired erectile function by altering nitric oxide activity in the penis. In addition, investigators examined the effect of testosterone on penile erection. In this study, animals were divided into five groups: sham-operated controls, castrated controls, castrates treated with testosterone, castrates treated with dihydrotestosterone, and castrates treated with a combination of testosterone and a 5 alpha reductase inhibitor. 5 alpha reductase inhibitors caused both a decrease in nitric oxide activity in the erection tissue and a reduction in erectile response to electrical stimulation.
I've seen Mens Rea mentioning Dr. Goldstein in the same sentence as Dr. Irwig, Shippen and Crisler. It appears like he's talking about the rat study I linked to in this thread. It seems like the proposition is based on that study.Irwin Goldstein
The pathophysiology of 5 alpha reductase inhibitors on sexual function may be related to reduction of dihydrotestosterone levels. Nitric oxide and the enzyme, nitric oxide synthase are critically important in sexually stimulated penile erections. Dihydrotestosterone is more potent than testosterone in raising nitric oxide synthase activity. Because 5 alpha reductase inhibitors reduce serum levels of dihydrotestosterone, this effect may be responsible for erectile dysfunction by reducing levels of nitric oxide and reducing nitric oxide synthase activity in the penile erection tissues.
Researchers have documented that at high doses, finasteride impaired erectile function by altering nitric oxide activity in the penis. In addition, investigators examined the effect of testosterone on penile erection. In this study, animals were divided into five groups: sham-operated controls, castrated controls, castrates treated with testosterone, castrates treated with dihydrotestosterone, and castrates treated with a combination of testosterone and a 5 alpha reductase inhibitor. 5 alpha reductase inhibitors caused both a decrease in nitric oxide activity in the erection tissue and a reduction in erectile response to electrical stimulation.
Enden said:I've seen Mens Rea mentioning Dr. Goldstein in the same sentence as Dr. Irwig, Shippen and Crisler. It appears like he's talking about the rat study I linked to in this thread. It seems like the proposition is based on that study.Irwin Goldstein
The pathophysiology of 5 alpha reductase inhibitors on sexual function may be related to reduction of dihydrotestosterone levels. Nitric oxide and the enzyme, nitric oxide synthase are critically important in sexually stimulated penile erections. Dihydrotestosterone is more potent than testosterone in raising nitric oxide synthase activity. Because 5 alpha reductase inhibitors reduce serum levels of dihydrotestosterone, this effect may be responsible for erectile dysfunction by reducing levels of nitric oxide and reducing nitric oxide synthase activity in the penile erection tissues.
Researchers have documented that at high doses, finasteride impaired erectile function by altering nitric oxide activity in the penis. In addition, investigators examined the effect of testosterone on penile erection. In this study, animals were divided into five groups: sham-operated controls, castrated controls, castrates treated with testosterone, castrates treated with dihydrotestosterone, and castrates treated with a combination of testosterone and a 5 alpha reductase inhibitor. 5 alpha reductase inhibitors caused both a decrease in nitric oxide activity in the erection tissue and a reduction in erectile response to electrical stimulation.
epro said:Yesterday, i was almost complety fine, today my penis is again smaller, shrinking, but my libido, erections are completely normal. What the f*ck is going on?
monty1978 said:Mens Rea said:epro said:Yesterday, i was almost complety fine, today my penis is again smaller, shrinking, but my libido, erections are completely normal. What the f*ck is going on?
Fluctuations. There is something going on in your body.
I can go from almost normal to completely dysfunctional inside a day. One day i have a good sized penis the next day its pencil dick. No joke.
I'm the same. I am getting better though after considerable time. It does get better guys for most anyway.
Mens Rea said:My penis and semen had been excellent there for a few weeks. Then after two nigths drinking things went south, massively. It just showed me that my body isn't at 100% and doing unhealthy things put it back into retreat. I'll be looking after myself in a very specific way in the coming weeks. Will report back.