and then we start killing most of the dht in our bodies with finasteride...so what happens now...do we still run the risk of turning into hermaphrodites
Not exactly -- with finasteride you are changing your hormonal profile to match that of a pseudohermaphrodite, after puberty. Others like Pondle may argue that this is perfectly acceptable since we have a biological example -- those pseudo's with 5AR2 defiency -- that seem to "live" perfectly normal lives despite the absence of 5AR-II -- but what about for the rest of us who don't have mutated 5AR-II enzymes? With finasteride we are instilling a
surrogate state of 5AR2 deficiency in otherwise healthy, normal human beings that were never meant to operate as such from birth... a situation from which the consequences can lead to numerous problems/side effects it seems, both while on and after quitting the drug, for some.
why does finasteride work to stop male pattern baldness for some humans whereas for others it has no effect?
Likely due to genetics of each person, some are more prone to the effects of finasteride while others are not. There are studies that corroborate this, ie
Effectiveness of Finasteride on Patients with Male Pattern Baldness Who Have Different Androgen Receptor Gene Polymorphism
http://www.nature.com/jidsp/journal/v10 ... 0229a.html
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Most male pattern baldness (male pattern baldness) patients have an androgen-dependent trait, although it is thought to be under the control of multiple genes, such as genes for androgen receptor (AR), insulin-like growth factor-1 (IGF-1), and dihydrotestosterone regulations (Nyholt et al, 2003;Tang et al, 2003).
One of the 5 -reductase inhibitors, finasteride, is effective on male pattern baldness, although there is a variation in the efficacy of this drug among the male pattern baldness patients. From the functional mechanism of this drug, it is thought to be effective on the male pattern baldness caused by hyperfunction of AR.
Association of higher incidence rate of male pattern baldness with lower triplet repeat number in the first exon of AR gene has been demonstrated by some authors (Sawaya and Shalita, 1998;Ellis et al, 2001).
Tracing their study, we have found that there is a correlation between the symptom levels of male pattern baldness and the CAG and GGC repeat numbers in AR gene.1 To
investigate the relationship between the effectiveness of finasteride and the AR gene polymorphism, we determined the number of triplet repeats in AR gene of patients.
Effectiveness of finasteride on each patient was expressed as the improvement point of symptom derived from the modified Hamilton–Norwood typing. The number of the triplet repeats (CAG+GGC) was plotted against the symptom points.
There was a broad correlation between these variables Figure 1.
The smaller the repeat number, the higher the improvement with finasteride.
Patients were divided into two groups: the group comprised of patients whose number of repeats was 40 or less, and the group of more than 40. Larger number of patients in the former group (40) obtained higher improvement points, compared with that in the latter (>40) (data not shown). [
Finasteride was more effective on patients in the short repeat group (40); even they had severe initial symptoms (V–VII). The relation between the improvement points and total dose of fnasteride was analyzed.
In the shorter repeat group (40), their mean improvement point was 0.96 to 1.1 even by a smaller total dose, 30–100 mg, while 200 mg or more was necessary to achieve the same improvement in the long repeat group (>40). Finasteride was less effective on patients in the long repeat group (>40) especially on patients younger than 30 y.
As mentioned above,
we have found that the shorter the CAG and GGC repeat numbers, the higher the symptom level before treatment with finasteride. Although, the mean initial symptom of patients in the short repeat group was worse,
finasteride was more effective in the improvement of male pattern baldness in most patients with shorter triplet regions of AR gene. These cases may be caused by hyperfunction of AR. On the other hand, this drug was less effective in certain cases with longer triplet repeats. They are thought to result from a non-androgenic mechanism. This kind of analysis may aid in the choice of drug for male pattern baldness patients.
Graph showing effect of finasteride on patients with different triplet repeat numbers in androgen receptor (AR) gene:
http://www.nature.com/jidsp/journal/v10 ... gure-title