Update:
Finasteride vs Dutasteride study:
This study compared the inhibition of different genetic variants of 5-alpha reductase type II by both finasteride and dutasteride. 5-alpha reductase type II is the enzyme responsible for converting testosterone into dihydrotestosterone (DHT). It’s present in both the prostate and the skin and hair follicles. Increased DHT and/or increased sensitivity towards it had been linked to both male pattern baldness (male pattern baldness) and prostate cancer. Perhaps not surprisingly there’s also a link between male pattern baldness and prostate cancer.
Finasteride and dutasteride are both competitive inhibitors of 5-alpha reductase type II (though dutasteride also inhibits 5-ar type I), meaning that they compete with testosterone in binding to it. If finasteride or dutasteride binds to the enzyme then testosterone can’t and no conversion to DHT can be performed by that enzyme molecule for as long as the inhibitor is in place. Both substances are used to treat an enlarged prostate. Finasteride has also been used as a prostate cancer preventative medication. It’s sold in a 5mg pill under the name Proscar to treat enlarged prostates and in a 1mg version under the name Propecia as a hair loss treatment.
The gene coding for 5-alpha reductase exists in several different forms and some variants affect both the incidence and the progression of cancer in the prostate. In this study the effect of finasteride and dutasteride was measured on several constitutional and somatic genetic variants of 5-alpha reductase type II. Constitutional cells are germ-line cells, meaning sperms and eggs, somatic cells are all other cells in the body. In this case the somatic cells were cancer cells from the prostate.
The result was that the genotype of the 5-alpha reductase type II enzyme governed how effective the inhibition was, and furthermore it showed that while dutasteride was a more effective inhibitor in most cases, that wasn’t true in all of them. How different genotypes govern the effectiveness of a pharmaceutical is called pharmacogenetics. A genetic difference in an enzyme doesn’t have to mean that it’s affected differently by a drug per se, but when it is, it’s said to be phamacogenetically as well as genetically different.
The study also demonstrated that both finasteride and dutasteride are slow, time-dependent inhibitors, meaning inhibition is lower at first but increases with time.
Dutasteride was shown to be more effective and showed less variation in inhibition of the different genotypes of 5-alpha reductase type II than finasteride. In a few genotypes, finasteride showed better inhibition than dutasteride, indicating that genotyping of patients would be beneficial when choosing treatment. This also provides a possible answer as to why some people who treat their hair loss with finasteride see a lot of improvement when they switch to dutasteride, and why a few instead notice a worsening of their condition. It may very well be due to some genotypes responding better to one drug than the other.
From a statistical standpoint, dutasteride is more likely to provide better results, but if finasteride seems more effective for you, despite the theoretically lower inhibition, then you might benefit from sticking to it after all.
http://www.hairlosshelp.com/hair_loss_n ... mmentID=43
:study:
ensativo:
