Positive/Negative Effects of Normal/High DHT on Metabolic Pathways

Regular visitors of the SuppVersity will certainly remember some of my previous posts about the false demonization of DHT. A new study coming from the Institute of Endocrinology in Prague (Duskova. 2010) supports the view that "optimal" and not low DHT levels are what men should be striving for.

Theorizing that DHT as a non-aromatizable androgen could be responsible for a male type fat distribution, the scientists reviewed the results of both animal and human studies and found that "physiological levels of DHT [do not only] inhibit growth of mature adipocytes", but also have positive levels on body composition in patients on hormone replacement therapy (HRT). On the other hand, there is also evidence that high (super-physiological) DHT levels are associated with obesity:

In obese people, DHT metabolism in adipose tissue is altered. Local abundance of non-aromatizable androgen has a negative effect on adipose tissue and it could be involved in pathogenesis of metabolic and cardiovascular diseases.

So, in view of getting/staying lean and healthy, you want your DHT levels within normal ranges and you certainly don't want to block it by taking Saw Palmetto or (God forbid) Finasteride or other drugs out of fear of developing prostate cancer, even if you do not even know if your DHT levels are pathologically elevated.

Is DHT Really the 'Bad and the Ugly'?

Fellow men, common (bro-)science tells us that dihydrotestosterone (DHT, molecular structure see image on the right. HMDB) will make your hair fall out and trigger cancerous growth of your prostate. Current research, however, suggests that Estrogen might just as well be the real culprit when it comes to unwanted growth a few inches above your testes. This is, as Williams (2010) phrases it, part of a "controversial break-through" achieved by scientists in the course of the last months and the results of which he sums up as follows:

"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."