HairlossTalk
Senior Member
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New meaning 2004. What do you guys think about this?
Effectiveness of Finasteride on patients with male pattern baldness who have different Androgen Receptor Gene Polymorphism
Objectives:
Most of male pattern baldness (male pattern baldness) patients have androgen-dependent trait although it is under control of multiple genes, such as genes for androgen receptor (AR) IGF-1 and DHT (Dihydrotestosterone) regulations.
A 5alpha-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 male pattern baldness caused by hyper-function of androgen receptors.
Association of polymorphism in the first exon of androgen receptor gene with male pattern baldness has been demonstrated by some authors (Marty 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 leength in the Androgen Receptor gene. We want to investigate relationship between the effectiveness of finasteride and the Androgen Receptor gene polymorphism, we determined the number of triplet repeats in Androgene Receptor gene of patients.
Methods:
Blood Cell DNA was extracted from 740 male pattern baldness patients (age 19 to 62) and 54 men who were not losing their hair (age 44 to 72). After PCR of the first exon of their Androgen Receptor gene, the number of CAG and GGC triplets was determined by conventional sequencing or transcriptional sequencing method. AGGCCT sequence was determined using two different Stul restriction enzymes.
Results and Conclusions:
Effectiveness of Finasteride in each patient was defined as showing improvement on the Norwood scale. Number of the triplet repeats (CAG+GGC) was plotted against the symptom points. There was a broad correlation between these variables.
Finasteride was more effective for patients who had shorter triplet regions of the androgen receptor gene. Therefore hair loss may be caused by a hyper-function of the androgen receptors in these people. On the other hand, Finasteride was LESS effective when we found longer triplet repeats. These people may be losing their hair due to a non-androgenic related mechanism. This sort of analysis may help people choose what treatment to use for their Male Pattern Baldness.
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Now I could be wrong but my understanding is that they established (1) A reason why some people do not respond to Propecia (Finasteride) and (2) That some male pattern baldness is not necessarily Androgenic in nature (DHT is not the culprit). Apparently the difference between responders and non-responders was a notable difference in what they call the "hyper-function" of the androgen receptors. Not sure what this means...
Bryan?
Effectiveness of Finasteride on patients with male pattern baldness who have different Androgen Receptor Gene Polymorphism
Objectives:
Most of male pattern baldness (male pattern baldness) patients have androgen-dependent trait although it is under control of multiple genes, such as genes for androgen receptor (AR) IGF-1 and DHT (Dihydrotestosterone) regulations.
A 5alpha-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 male pattern baldness caused by hyper-function of androgen receptors.
Association of polymorphism in the first exon of androgen receptor gene with male pattern baldness has been demonstrated by some authors (Marty 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 leength in the Androgen Receptor gene. We want to investigate relationship between the effectiveness of finasteride and the Androgen Receptor gene polymorphism, we determined the number of triplet repeats in Androgene Receptor gene of patients.
Methods:
Blood Cell DNA was extracted from 740 male pattern baldness patients (age 19 to 62) and 54 men who were not losing their hair (age 44 to 72). After PCR of the first exon of their Androgen Receptor gene, the number of CAG and GGC triplets was determined by conventional sequencing or transcriptional sequencing method. AGGCCT sequence was determined using two different Stul restriction enzymes.
Results and Conclusions:
Effectiveness of Finasteride in each patient was defined as showing improvement on the Norwood scale. Number of the triplet repeats (CAG+GGC) was plotted against the symptom points. There was a broad correlation between these variables.
Finasteride was more effective for patients who had shorter triplet regions of the androgen receptor gene. Therefore hair loss may be caused by a hyper-function of the androgen receptors in these people. On the other hand, Finasteride was LESS effective when we found longer triplet repeats. These people may be losing their hair due to a non-androgenic related mechanism. This sort of analysis may help people choose what treatment to use for their Male Pattern Baldness.
---------------------
Now I could be wrong but my understanding is that they established (1) A reason why some people do not respond to Propecia (Finasteride) and (2) That some male pattern baldness is not necessarily Androgenic in nature (DHT is not the culprit). Apparently the difference between responders and non-responders was a notable difference in what they call the "hyper-function" of the androgen receptors. Not sure what this means...
Bryan?
