Propecia~Finasteride

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  1. #1
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    Propecia~Finasteride

    (Propecia, Proscar)



    Finasteride was available for years as Proscar (5mg tabs), but only recently became available as Propecia (1mg tabs). It is in a class of chemicals known as 5alpha-reductase inhibitors. It is based on the progesterone skeleton (4) and has a high inhibitory activity for the enzyme 5alpha-reductase (5-AR). 5-AR, as you may recall, is the enzyme responsible for converting certain steroids into 5-Alpha Reduced versions of themselves (such as turning testosterone into dihydrotestosterone). Finasteride and similar compounds are used for the treatment of androgen dependent diseases such androgenic alopecia (hair loss), benign prostatic hyperplasia (prostate enlargement) and prostate cancer. Dihydrotestosterone is a 5alpha-reduced metabolite of testosterone and has been implicated as a causative factor for the onset and progression of these problems. This was discovered when males who are genetically deficient of the enzyme steroid 5alpha-reductase were shown to have much lower incidences of these problems (1)(2). Of course, these problems can be a major annoyance, and nothing to toy around with, but by using finasteride you risk reducing your gains on a given cycle, and can even suppress reproductive function (3). I'm not a big fan of this, as you could guess. However, if you are worried about your hairline, or have incidences of prostate issues in your family, then 1mg/day of Finasteride may be the answer you've been looking for.

    It needs to be noted that there are actually 2 different 5-AR enzymes, and Finasteride specifically blocks the type-II variety. The type-II 5-AR enzyme is the one responsible primarily for hairloss and prostate enlargement, while type-I is often the culprit behind acne and hirsutism. In either case, type-II is responsible for around 2/3rds of the circulating DHT in your body, so it's no surprise that Finasteride typically reduces your total DHT levels by around 65%.

    There is also some novel information about this compound regarding the conversion of testosterone into DHT via the 5-Alpha-reducatase enzyme. It's come to my attention that the actual conversion process of testosterone into DHT via this enzyme may act in some way to inhibit luteinizing hormone release (and ergo would inhibit your HPTA and natural testosterone production). Check this out:


    Basically, this chart above shows the baseline level of LH in male sheep given a 5-Alpha-Reductase inhibitor (such as Finasteride), then one showing the LH levels in sheep given testosterone propionate, and finally a chart showing LH levels of sheep given testosterone propionate + the inhibitor (graph 3).(5) You'll note that although using the inhibitor alone produced no discernable effects on LH, when administered with testosterone, it seems to have allowed LH pulsality to continue nearly unaffected. This may indicate that you can use Finasteride on a cycle (1mg/day) and possibly keep your LH levels normal (and thus your HPTA), ergo making recovery much easier. This is, of course only my speculation.



    Reference:
    1. Steroidal antiandrogens and 5alpha-reductase inhibitors. Curr Med Chem. 2005;12(8):927-43.
    2. New 5alpha-reductase inhibitors: in vitro and in vivo effects. Steroids. 2005 Mar;70(3):217-24.
    3. [Effect of selective 5alpha-reductase inhibitor or/and testosterone undecanoate on the reproductive function of male rats] Zhonghua Nan Ke Xue. 2005 Jan;11(1):38-41. Chinese.
    4. New aromatic esters of progesterone as antiandrogens. J Enzyme Inhib Med Chem. 2004 Apr;19(2):99-105.
    5. Biology of Reproduction 50, 1244-50 (1994)

  2. #2
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    Finasteride-its impact on sexual function and prostate cancer.

    Anitha B, Inamadar AC, Ragunatha S.
    Department of Dermatology, Venereology and Leprosy, Shri B.M. Patil Medical College Hospital and Research Centre, Bijapur, Karnataka, India.
    Abstract

    Finasteride, a specific and competitive inhibitor of 5alpha-reductase enzyme Type 2, inhibits the conversion of testosterone to dihydrotestosterone (DHT). In adults, DHT acts as primary androgen in prostate and hair follicles. The only FDA-approved dermatological indication of finasteride is androgenetic alopecia. But, apprehension regarding sexual dysfunction associated with finasteride deters dermatologists from prescribing the drug and patients from taking the drug for androgenetic alopecia. Testosterone, through its humoral endocrine and local paracrine effects is relevant in central and peripheral modulation of sexual function than locally acting DHT. Several large population-based long-term placebo-controlled studies, using International Index of Erectile Function-5 questionnaire and objective method (Nocturnal Penile Tumescence) to assess the erectile function have demonstrated no clear evidence of the negative effect of finasteride on erectile function. Reduction in ejaculatory volume is the only established causal relationship between finasteride and sexual dysfunction. Though finasteride causes significant reduction in all the semen parameters except sperm morphology, they did not fall below the threshold levels to interfere with fertility. Therefore, the sexual adverse effects associated with finasteride should be viewed in relation to normal prevalence and natural history of erectile dysfunction in the population, age of the patient, other confounding factors and also nocebo effect. The impact of finasteride on the prevention of prostate cancer has been discussed extensively. Finasteride is found to be effective in significantly reducing the incidence of low-grade prostate cancer. But the paradoxical increase in high-grade cancer in the finasteride group has been attributed to increased sensitivity and improved performance of prostate specific antigen levels to detect all grades of prostate cancer.

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