The study recruited hypogonadal males between 18 and 60 years old who required T replacement therapy. The T plus D and D alone groups but not the T only group received a D loading dose of 24.5 mg, followed by 3 consecutive days of 0.25 mg D BID before starting the 28-day treatment phase. Subjects were randomized using a random number sequence to 1 of 5 treatments administered orally BID, including 1) 150 mg T plus 0.25 mg D, 2) 250 mg T plus 0.25 mg D, 3) 400 mg T plus 0.25 mg D, 4) 400 mg T alone or 5) 0.25 mg D alone. This randomized, open label, parallel group study consisted of a screening period, followed by a continuous 28-day treatment period (fig. 1). Current approved T therapies in the United States include injections, patches, gels, buccal tablets and oral alkylated T derivatives, eg methyltestosterone and oxandrolone.
Oral T administration in this study did not cause liver inflammation and most adverse events were minor. To our knowledge whether additional increases in metabolism would continue with longer treatment is unknown but for some medications this effect stabilizes with time. A drawback to our study was the relatively few men per group, the number who did not complete the study, and the lack of homogeneity in age and baseline T. Thus, future studies will focus on formulations with modified release characteristics for dose optimization to maintain Tavg in the normal range and maximum T below a reasonable level. There were no significant changes in hemoglobin and blood counts, serum chemistry, or markers of liver inflammation or PSA (data not shown). There were 16 nonserious adverse events without evidence of clustering to a specific treatment, of which the most common were headache, dizziness, upper respiratory infection, vomiting, back pain and frequent urination in 2 men each.
It is an analogue of androgen steroid hormones like testosterone and DHT. These metabolites show approximately 20% of the inhibitory activity of finasteride on 5α-reductase. At steady-state with 1 mg/day finasteride, mean peak concentrations of finasteride were 9.2 ng/mL (25 nmol/L). In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1). However, some authors do not define finasteride as an "antiandrogen," a term which can refer more specifically to antagonists of the androgen receptor. As such, finasteride is a type of antiandrogen, or more specifically, an androgen synthesis inhibitor.
The net androgen effect in any tissue can be viewed as a function of the prevalent intratissue testosterone and DHT concentrations and their relative androgenic potencies (eFigure 6). Furthermore, the relationship of testosterone concentrations with these outcomes did not differ between the dutasteride and placebo groups despite substantial differences in DHT concentrations. It is possible that conversion of testosterone to DHT is not obligatory, but that it amplifies the effects of testosterone in tissues with high 5α-reductase activity such as the prostate and skin, but not in tissues with low 5α-reductase activity such as skeletal muscle and bone.
Serum NTx (collagen-type I N-telopeptides) and osteocalcin levels did not change in the placebo and dutasteride groups. Increases in leg-press and chest-press strength were greater with larger doses and higher concentrations of testosterone. Leg-press and chest-press strength increased dependently by dose in the placebo and dutasteride groups. Luteinizing hormone levels were suppressed in the placebo and dutasteride groups. Thus, the study intervention was effective in creating 8 groups that had similar testosterone levels, but which differed in DHT levels. Secondary outcomes included fat mass, leg-press and chest-press strength, sexual function, sebum production, and prostate volumes, which were assessed at baseline and at week 20.
Finasteride has been used for the treatment of symptomatic benign prostatic hyperplasia (BPH) and for the treatment of male pattern hair loss. Adverse effects from finasteride are rare in men with already enlarged prostates; however, some men experience sexual dysfunction, depression, and breast enlargement. Gupta AK, Talukder M, Williams G. Comparison of oral minoxidil, finasteride, and dutasteride for treating androgenetic alopecia.
These are things I had to do anyways just as frequently before when I had normal amounts of DHT in my body. The entirety of the experiment I had zero DHT, but I still experienced facial hair growth and had to shave my face just as often. I thought okay great, so I can just use more Testosterone and keep all of my hair because DHT is still absent regardless of how much my Testosterone goes up. Even with a supraphysiological amount of Testosterone in my system from administering an exogenous a source of it and pushing my Testosterone up to 2,000 ng/dL (on purpose) I still had nearly zero DHT in my system because Dutasteride is just that effective at inhibiting 5-alpha reductase. While using Finasteride, you can reduce systemic DHT by roughly 70%, but you will still have 30% of your systemic DHT left in tact, which is still going to wreak havoc on your hair (common knowledge). Otherwise it would be helpful to prevent the progress of prostate size by TRT. However, prostate volume decreased significantly (Pvs. T +0.6 cc).
And, he also started re-growing scalp hair and reversing his male pattern baldness. The result of that was significant inhibition of facial hair and body hair growth. When he transitioned from male to female, he used oral estradiol and spironolactone. But, the problem with that is that by fulfilling those very androgen dependent physiological functions; you will also miniaturize hair follicles.
The incidence of prostate cancer was reduced (25% compared to placebo) in long-term studies with 5α-reductase inhibitors. Dihydrotestosterone is the most potent natural androgen with effects on numerous organs, especially during fetal development. A challenge to the development of oral T therapy has been the observation that oral T administration tends to induce its own metabolism by the liver, leading to a decrease in the resulting serum T with time.20,21 We observed a significant decrease in serum T with continued dosing of oral T during the 28-day treatment period, which was minimized by concomitant D administration. Also, oral T decreased SHBG during treatment, which contributed to the decrease in total T observed at the end of the study period.