i assume that finastride would prevent acne during a cycle with DHT converting steriods, considering it's a DHt blocker. since acne is caused by an increase in the seb glands, wich is caused by DHT, it makes sense. what do you guys think. :scratch:
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i assume that finastride would prevent acne during a cycle with DHT converting steriods, considering it's a DHt blocker. since acne is caused by an increase in the seb glands, wich is caused by DHT, it makes sense. what do you guys think. :scratch:
i did take finasteride before, during and after cycle and only got a little on my shoulder/back during pct, but not much really at all. that was test only @ 600mg/wk.
test usually makes me break out bad on my back. no signs at all and i'm approaching wk 4. maybe i'm still a little early for assumtions but i think the finast is helping...1g ed
nopeQuote:
Originally Posted by testosterona
finasteride blocks only 5-alpha reductase (5-AR) isozime 1,
dutasteride both (1-2)
bump for more opinions.
Finasteride may be useful for much more:
http://www.avantlabs.com/magmain.php...404&issueID=33
there is two 5 ar isoenzymes,dutasteride block both ,Quote:
Originally Posted by testosterona
finasteride just block type 1 (scalp tissue).
acne is type 2 .
5 alpha-Reductase Isoenzyme Inhibition
Both dutasteide and finasteride are 4-azasteroid inhibitors of 5 a -reductase , the enzyme responsible for converting testosterone to dihydrotestosterone (DHT) in the prostate. DHT is the primary androgen int the prostate and has a major role in the development and progression of benign prostatic hyperplasia (BPH) and other prostate diseases (1,2,3,4) as well as androgenetic alopecia (5,6).
Two isoenzymes of 5 a -reductase exist (type 1 and type 2). Type 2 is the dominant isoenzyme in genital tissues including the prostate, but is also present in the skin and liver. Type "1" 5 a -reductase is also found in the skin, liver and prostate, and is the dominant form in sebaceous glands. (1,2,4).
Finasteride is a competitive inhibitor of 5 a -reductase that selectively inhibits the type 2 isoenzyme, with which it forms a stable enzyme complex. this selective activity is attributed to a much lower affinity for the type 1 isoenzyme, and thus a slow rate of type 1 isoenzyme inhibition. In contrast, dutasteride is a competitive inhibitor of both forms of the enzyme, with 45-fold greater potency than finasteride against type 1 and type 2 isoenzymes at clinically used doses. this dual inhibition may potentially be beneficial in prostatic diseased that depend on androgens, since both isoenzymes are up-regulated in BPH while only the type 1 isoenzyme is up-regulated in prostate cancer, as noted above (2,1).
Pharmacogenetic analysis of human steroid 5 alpha reductase type II: comparison of finasteride and dutasteride.
Makridakis N, Reichardt JK.
J Mol Endocrinol. 2005 Jun;34(3):617-23.
An update on the use of 5 alpha-reductase inhibitors.
Foley CL, Bott SR, Shergill IS, Kirby RS.
Drugs Today (Barc). 2004 Mar;40(3):213-23. Review.
Acne is much more complicated than DHT. Ever notice that teenager girls get acne, too?
have high levels of testosterone.Quote:
Originally Posted by mranak
Archives of Dermatology. 2005 Mar;141(3):333-8.
Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women.
Cappel M, Mauger D, Thiboutot D.
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Am J Clin Dermatol. 2002;3(8):571-8.
Acne: effect of hormones on pathogenesis and management.
Shaw JC.
Division of Dermatology, University of Toronto, Toronto Western Hospital, 355 Bathurst Street EW 8-517, Toronto, M5T 258 Ontario, Canada. [email protected]
In the pathogenesis of acne, androgen hormones play a crucial role. In the treatment of acne, hormonal therapies provide valuable alternatives to standard modalities in selected women. Although numerous factors contribute to the development of acne, the requirement for androgens is absolute and is one that allows for effective treatments in women through inhibition of androgen expression. The two prerequisites for androgen expression at the level of the pilosebaceous unit are the presence of androgen in the form of either testosterone or dihydrotestosterone; and functioning androgen receptors. A third component may be the metabolism of androgen precursors to active androgens within pilosebaceous units.
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J Steroid Biochem Mol Biol. 2004 Jan;88(1):1-16.
Selective non-steroidal inhibitors of 5 alpha-reductase type 1.
Occhiato EG, Guarna A, Danza G, Serio M.
Dipartimento di Chimica Organica Ugo Schiff, Polo Scientifico Universita di Firenze, Via Della Lastruccia 13, I-50019 Sesto Fiorentino, Florence, Italy.
The enzyme 5 alpha-reductase (5 alpha R) catalyses the reduction of testosterone (T) into the more potent androgen dihydrotestosterone (DHT). The abnormal production of DHT is associated to pathologies of the main target organs of this hormone: the prostate and the skin. Benign prostatic hyperplasia (BPH), prostate cancer, acne, androgenetic alopecia in men, and hirsutism in women appear related to the DHT production. Two isozymes of 5 alpha-reductase have been cloned, expressed and characterized (5 alpha R-1 and 5 alpha R-2). They share a poor homology, have different chromosomal localization, enzyme kinetic parameters, and tissue expression patterns. Since 5 alpha R-1 and 5 alpha R-2 are differently distributed in the androgen target organs, a different involvement of the two isozymes in the pathogenesis of prostate and skin disorders can be hypothesized. High interest has been paid to the synthesis of inhibitors of 5 alpha-reductase for the treatment of DHT related pathologies, and the selective inhibition of any single isozyme represents a great challenge for medical and pharmaceutical research in order to have more specific drugs. At present, no 5 alpha R-1 inhibitor is marketed for the treatment of 5 alpha R-1 related pathologies but pharmaceutical research is very active in this field. This paper will review the major classes of 5 alpha R inhibitors focusing in particular on non-steroidal inhibitors and on structural features that enhance the selectivity versus the type 1 isozyme. Biological tests to assess the inhibitory activity towards the two 5 alpha R isozymes will be also discussed.