"The synergistic action of unopposed oestrogen and leptin, compounded by increasing insulin, cortisol and xeno-oestrogen exposure directly initiate, promote and exacerbate obesity, type 2 diabetes, uterine overgrowth, prostatic enlargement, prostate cancer and breast cancer."It was thus certainly no bodily injury caused by negligence, when Konnelius et.al. 2002 administered 125-250mg transdermal DHT to 60 subjects (age range, 50–70y) and found:
"Early morning erections improved transiently in the DHT group at 3 months of treatment (P < 0.003), and the ability to maintain erection improved in the DHT group compared with the placebo group (P < 0.04). No significant changes were observed in general well-being between the placebo and the DHT group. Serum concentrations of LH, FSH, E2, T, and SHBG decreased significantly during DHT treatment. Treatment with DHT did not affect liver function or the lipid profile. Hemoglobin concentrations increased from 146.0 ± 8.2 to 154.8 ± 11.4 g/liter, and hematocrit from 43.5 ± 2.5% to 45.8 ± 3.4% (P < 0.001). Prostate weight and prostate-specific antigen levels did not change during the treatment. No major adverse events were observed."Another article published in The Journal of Clinical Endocrinology & Metabolism by Wang, et.al. (2002) explicitly mentions the anti-carcinogenic effect of DHT in older men:
"In older men (55–70 yr of age), DHT surprisingly resulted in improved sexual function and a small (15%) decrease in prostate volume (29). The effects on the prostate appear to be counter intuitive because DHT is the principal androgen required for the growth of the prostate. One hypothesis for the decrease in prostate size after DHT treatment of older hypogonadal men is based on the observation that estrogens may act synergistically with androgens in the prostate to promote prostate growth (30, 31, 32, 33, 34). DHT may lower tissue E2 levels by at least two mechanisms."In their review on the possible use of DHT for the treatment of andropause (i.e. the male equivalent to menopause) Wang, et.al. (2002) also report on DHT's effects in younger subjects:
"Because DHT is not converted to estrogens, DHT would not cause gynecomastia while providing androgenic effects. It is an ideal replacement therapy for patients with 5-alpha reductase 2 deficiency (11, 12). It is potentially useful for the treatment of pubertal gynecomastia (24, 25), microphallus (26), and constitutional delayed puberty in boys. [...]
In hypogonadal men, transdermal DHT gel treatment has been reported to maintain sex characteristics, increase muscle mass, and improve sexual function without significant increases in prostate size (27, 28)."While these news should by no means encourage you to supplement additional DHT, they should however make you reconsider the usefulness of supplements such as saw palmetto or even the (ab-)use of drugs as finasteride without medical indication.
So keep in mind Ori Hofmeklers (author of The Warrior Diet) words in Maximum Muscle Minimum Fat: The Secret Science Behind Physical Transformation (Hofmekler. 2008. p.32):
"Testosterone is regarded the most anabolic male steroid hormone. 'Big T', however, isn't as big as it seems. In fact, some researchers consider testosterone to be a prohormone because of its relatively weak actions compared to other androgens, in particular DHT."UPDATE: Obviously, some of you are still concerned about benign prostate hyperplasia. I must admit that I do not own a copy of the books cited Konnelius, et.al. - I was however able to find other references to the studies cited speaking of "no observable [ultrasound] effect on prostate size". The fact that the use of DHT as an agent to fight benign prostate hyperplasia has been patented in 1997 may also be considered as additional evidence that even back in the days, people knew that excess estrogen is the real fallacy.