Study looking at why Propecia is only effective for some

[jambri]

Journal of Investigative Dermatology Symposium Proceedings

Effectiveness of Finasteride on Patients With Male Pattern Baldness Who Have Different Androgen Receptor Gene Polymorphism
Kazuhiro Kobayashi, Nagaoki Wakisaka, Yuh-ichi Taira, Masahiro Ishikawa, Yoshio Nakamizo,
Masashi Uwabu, Yasutaka Fukuda, Yasuyuki Taguchi, Takanori Hama, and Masaya Kawakami
NPO Future Medical Laboratory, Tokyo, Japan

Objectives: Most of male pattern baldness (male pattern baldness) patients have androgen-dependent trait although it is under the control of multiple genes, such as genes for androgen receptor (AR), IGF-1 and dihydrotestosterone regulations. A 5 alpha-reductase inhibitor, 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 MBP caused by hyper-function of AR. Association of polymorphism in the first exon of AR gene with male pattern baldness has been demonstrated by some authors (Sawaya and Salita, 1998; Ellis et al,
2001).We have found that there is a correlation between the symptom level of male pattern baldness and the CAG and GGC repeat length in AR gene. To investigate relationship between the effectiveness of finasteride and the AR gene polymorphism, we determined the number of triplet repeats in AR gene of patients.

Methods: Blood cell DNA was extracted from 740 male pattern baldness patients (19–62 y) and 54 non-bald men (44–72 y). After PCR of the first exon of AR gene, the number of CAG and GGC triplets was determined by conventional sequencing or transcriptional sequencing method. AGGCCT sequence was determined using two different Stu I restriction enzymes.

Results and Conclusions: Effectiveness of finasteride in each patient was expressed as the improvement point of symptom derived from Hamilton-Norwood typing. Number of the triplet repeats (CAGþGGC) was plotted against the symptom points. There was a broad correlation between these variables. Finasteride was more effective for the improvement of male pattern baldness in 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 non-androgenic mechanism. This sort of analysis may help the drug choice for male pattern baldness patients.

 

[westcovinajoe]

From that I think it says that if in fact a guy is taking it because he suffers from DHT related male pattern baldness, then Propecia will work. If not then it won't.

Maybe someone can help us translate if I am wrong...

 

[Subliminal]

From that I think it says that if in fact a guy is taking it because he suffers from DHT related male pattern baldness, then Propecia will work. If not then it won't.

Maybe someone can help us translate if I am wrong...

Not quite. What it's saying is that different people have slighty different variations of the androgen receptor. Some people have very "sensitive" ARs, which means even low concentrations of androgens like DHT induce strong physiological responses, such as atrophy of the hair follicle. Sort of like how people have slighty different shades of skin pigment, which correlates with susceptibility to UV light.

finasteride doesn't remove all DHT. The little DHT left over can still have a very strong physiological effect in people with "sensitive" ARs. These people do not improve much with finasteride treatment as a result. The only way to improve hairloss in such guys is probably hair transplant.

 

[jeffsss]

well when are they going to be able to test patients?
I hate to be changing my hormones and wasting money for nothing. :-x

 

[Britannia]

That explains why people respond differently to finasteride i.e. maintenance, mild regrowth, moderate regrowth etc. It doesnt explain why some people (14%) have absolutely NO response to treatment.
I believe the reason for this 14% "failure" of finasteride lies with Pharmacodynamics i.e. the breakdown and absorption of the drug once taken. Some people do not correctly metabolise or absorb the drug and therefore the finasteride simply passes through the body without expressing any effect on DHT production. This is only my theory, but it would certainely explain the observed 14% failure rate.