I am not convinced at all.
It is stated that testosterone converted by 5 alpha reductase into DHT is the cause, therefore inhibiting testosterone or 5 alpha reductase (finasteride) is the solution.
How come that BPH usually is a concern when testosterone levels are well declined?
After about 30 years of age testosterone levels start to decline and estrogen to rise, it is quite rare to hear of BPH before 50.
To me it makes much more sense to believe it is the decline in testosterone and the concomitant rise in estrogen that causes it.
It seems lowering estrogen is controversial in reducing BPH with some research finding no such effect, but it is a fairly new approach (by the medical community) and not much research has been done yet, I suggest keeping an eye on it since dismissing this wouldn't be justified (yet, at least).
Saw palmetto "should" work on the same principles but is much milder (more later).
Nettle root works on different pathways (including estrogen inhibition) and might be preferable.
http://www.progressi...-swollen-pr.htm
Epilobium parviflorum is not well known outside Germany and Austria but is very effective and probably first choice, it works on different pathways including relatively strong estrogen inhibition.
In my view the strategy should be to rise testosterone, lower estrogen (especially estradiol), avoid messing up with drugs (finasteride) and help with epilobium and maybe nettle root (both as tea).
About saw palmetto:
Saw palmetto, specifically the n-hexane extract, seems to inhibit both isomers of the 5α-reductase enzyme at concentrations which approximate plasma concentrations reached via oral ingestion of the supplement. These inhibitory effects have been shown to reduce DHT formation in vitro, and while less potent it is seems to be comparable in efficacy to finasteride. It is not certain what molecule(s) mediate this effect, as the potency seen in some extracts is far greater than the dietary fatty acids present in saw palmetto.
It has been noted in prostate cancer cells (LNCaP) that, while finasteride suppresses the activity of the type II isomer of 5α-reductase alongside other effects (suppression of PSA secretion and downregulation of prostatic androgen receptors), saw palmetto failed to downregulate the androgen receptor or influence PSA secretion rates.
Studies assessing saw palmetto on testosterone are currently highly confounded with other nutrients or have potential conflicts of interest. One lone study lasting only a week using saw palmetto in isolation failed to find any influence on testosterone or DHT concentrations.
http://examine.com/s...s/Saw Palmetto/
Again it seems that is not reducing DHT that elicits a positive effect on BPH, other mechanism are likely to come in play (estrogen inhibition mainly but not only).
Trowing saw palmetto in the mix might work, for sure it will not negatively effect your training, guaranteed.
Weight gain (likely water retention), reduced sex drive and reduced motivation in the gym points to low testosterone, high estrogen and possibly high cortisol (low DHT too is likely to cause water retention and that is probably the finasteride).
Having those tested might give you some insight.
If testosterone replacement is chosen make sure to check very often estrogen levels and eventually avoid high levels (aim for the lower limits) with anastrozole under medical supervision, of course.
Anastrozole alone might help with both low testosterone and BPH, again testing often and under medical supervision only since drugs tend to be little forgiving.
