Internal sides like Prostate enlargement are very debatable as far as what the direct cause is. So I think a little more understanding is needed for beginners and all thinking about undertaking AAS and especially 5-alpha reductase blockers like Finasteride. Most valid studies point to estrogen as being one of the biggest contributers. Certain steroids like Trenbolone are notorious for prostate enlargement and people think; wait it's not DHT, doesn't convert to DHT, so it must be that DHT is so androgenic and Trenbolone is 5x as androgenic as Test; so it's the androgenic effect that causes it. Well, just like blaming DHT, blaming androgeniccy is also a fallacy and not the complete story. Some steroids bind to the androgen receptors in the prostate more than others, not only that, but independant of it's ability to bind to the AR some are more "active" Take Deca for instance, it binds much stronger than Test or DHT to the prostate's androgen receptors but exerts very little effect and actually in theory blocks other more "active" steroids from binding. DHT does bind very well and does have activity at the prostate AR, but studies done with supplimenting DHT actually have shown prostate size reversal even with supraphysiological levels, showing that perhaps the actual conversion is what might be the cause or more than likely the reduced estrogen from the DHT displacing it causing reduction and in other cases hypertrophy. I'm rambling so I'm out for now.