Are higher does of Minoxidil more effective?

[IDOASIS]

Testosterone ability to possibly cause male pattern baldness, as well, is most concerning to me as it could be one of two reasons why drugs like propecia and avodart prove useless in the long run as some DHT still binds and testosterone will always be there to keep the disease progressing. But, that's just my opinion.

Doctor,
I know its true concerning propecia,
but why do you think avodart has prove useless in the long run.

 

[docj077]

Testosterone ability to possibly cause male pattern baldness, as well, is most concerning to me as it could be one of two reasons why drugs like propecia and avodart prove useless in the long run as some DHT still binds and testosterone will always be there to keep the disease progressing. But, that's just my opinion.

Doctor,
I know its true concerning propecia,
but why do you think avodart has prove useless in the long run.

Because, testosterone still causes male pattern baldness, but at a slower rate. DHT inhibition is not enough for a person to maintain the hair they have indefinitely. Especially, if they have strong genetics working against them.

 

[CCS]

that leaves two options: stop testosterone from binding with the androgen receptor, or use topicals that stop its downstream products. I prefer to do both, and as cheaply as I can.

Even castration only gets rid of 95% of both androgens. That's way better than propecia, which gets rid of less than 90% of DHT.

 

[IDOASIS]

It's obviously possible that a given treatment effective at treating AA could also be effective at treating male pattern baldness (minoxidil is an obvious example), but what does that have to do with azelaic acid? We don't even know how it (supposedly) works for AA, so why are you so convinced that it's going to have anything like a similar effect on male pattern baldness?

Bryan ,
How many drugs/topicals are you familiar with ,which are useful
for AA but not male pattern baldness?

Were you using it in the form of Xandrox?

I have never used Dr Lee products ,
I refuse to pay his ridiculous prices.

I'm glad that you think it helped you, but did it REALLY?

I have been using minoxidil since 1999.
2002-2003-propecia.
April 2005 until today -avodart.
I added AZELAIC ACID 20% (at the temples) 3 months after I have started avodart.
April 2006 -I changed my minoxidil 5% to genhair 15% .


I have seen a significant regrow at the hairline few months after I added
azelaic acid 20%.
At December 05 I have stopped using azelaic acid and saw a deteriorate at the temples.
I'm still trying to recover my temples using minoxidil 15% , with only a partial success.

APRIL 2005:

December 2005:

 

[IDOASIS]

Because, testosterone still causes male pattern baldness, but at a slower rate. DHT inhibition is not enough for a person to maintain the hair they have indefinitely. Especially, if they have strong genetics working against them.

So how could it be that at the firsts few years there can be an improvement.
Well I think its just a speculation.
I dont know a study which can confirm avodart is useless in the long run,
whereas there is a study which confirm avodart inhibits more DHT in the long run.

A total of 4325 men were randomized into the double-blind phase of the studies: 2158 to placebo and 2167 to dutasteride (Figure 1). For the open-label phase, 2340 patients were enrolled; 1188 had previously received dutasteride (D/D group) and 1152 had previously received placebo (P/D group). Figure 1 shows that for the P/D group, 67% and 70% completed the 2 phases of the study (24 and 48 months, respectively), versus 70% and 73% in the D/D group. Table 1 includes data for patients from the open-label ITT population. No significant differences at the start of the double-blind phase in baseline parameters were observed between patients in the D/D group and those in the P/D group, except for higher mean Qmax values in the P/D group. To exclude the possibility of responder bias in the open-label extension phase of the study, the characteristics of the men who entered the open-label phase were compared with those who elected not to continue with the study, and were found to be comparable in all parameters (Table 2).

Patients in the D/D group experienced a median decrease in DHT concentration of 93.7% from baseline to month 24, which was maintained to month 48 (95.3%). Patients in the P/D group had a median 5.9% increase at month 24 and a 95.4% decrease at month 48. At this timepoint, 87% of patients in the D/D group and 89% of patients in the P/D group had a reduction in DHT ≥ 90%.

From baseline to month 24, patients treated with dutasteride had a mean reduction in TPV of 26.0% versus a mean increase of 1.4% for placebo-treated patients (P < .001 between treatment groups) (Figure 2A). At month 48, patients who had been switched from placebo to dutasteride at month 24 (P/D group) had a reduction from baseline in TPV of 21.7%, which was significant versus month 24 (P < .001). TPV continued to decrease from months 24 to 48 for D/D-treated patients, although this decrease was not statistically significant (P = .07). The overall reduction in TPV from baseline to month 48 in D/D-treated patients was significantly greater than that observed in P/D patients (−27.3%, P < .001). Transition zone volume (TZV) decreased in the D/D patients by 20% at 48 months, versus 14.2% in the P/D patients (Figure 2B). However, the P/D-treated patients experienced an increase by nearly 10% from baseline to 24 months prior to being switched to dutasteride.

From baseline to month 24, patients treated with dutasteride had a mean reduction in AUA-SI score of 4.4 points versus 2.5 points for placebo-treated patients (P < .001 between treatment groups) (Figure 3). At month 48, patients who had been switched from placebo to dutasteride at month 24 (P/D group) had a reduction from baseline in AUA-SI score of 5.6 points, which was significant versus month 24 (P < .001). AUA-SI score decreased significantly from months 24 to 48 for D/D-treated patients (P < .001), with the overall reduction from baseline significantly greater than that observed in patients from the P/D group (6.5 points, P < .001).

 

[joseph49853]

Nice results IDOASIS. In the end, it's whatever works personally for you.

And no offense guys, but this conversation sounds as if being made by a bunch of junior Google scientists looking for a lab. The studies are flying fast and furious without a unifying or empirical standard, or single control running throughout. These broad conclusions just don't elevate enough to pack any punch for me. Almost like a pissing match you'd find in any bar or Internet cafe anywhere across the globe.

 

[LookingGood!]

Nice results IDOASIS. In the end, it's whatever works personally for you.

And no offense guys, but this conversation sounds as if being made by a bunch of junior Google scientists looking for a lab. The studies are flying fast and furious without a unifying or empirical standard, or single control running throughout. These broad conclusions just don't elevate enough to pack any punch for me. Almost like a pissing match you'd find in any bar or Internet cafe anywhere across the globe.

Agreed, I do think the regrowth was mostly from the avodart. The original thread content was if higher does of minoxidil were more effective and it became a pissing match regarding Alopecia areata/genetics/etc.

How about we all move back on topic?

 

[LookingGood!]

that leaves two options: stop testosterone from binding with the androgen receptor, or use topicals that stop its downstream products. I prefer to do both, and as cheaply as I can.

Even castration only gets rid of 95% of both androgens. That's way better than propecia, which gets rid of less than 90% of DHT.

You're not considering castration are you? :lol:

 

[docj077]

Because, testosterone still causes male pattern baldness, but at a slower rate. DHT inhibition is not enough for a person to maintain the hair they have indefinitely. Especially, if they have strong genetics working against them.

So how could it be that at the firsts few years there can be an improvement.
Well I think its just a speculation.
I dont know a study which can confirm avodart is useless in the long run,
whereas there is a study which confirm avodart inhibits more DHT in the long run.

Histologically, I don't believe that it has ever been shown that an improvement in scalp conditions occurs while on propecia and avodart. male pattern baldness continues while drugs like propecia and avodart cycle your hair using IGF-1 as a growth factor until the fibrosis that accompanies hair loss overwhelms even the growth stimulatory molecules that were helping you not only maintain your hair, but grow hair, as well. Studies clearly show that IGF-1 is upregulated while on 5AR inhibitors.

 

[powersam]

aside from your little discussion going on here, congrats on the regrowth idoasis.

 

[IDOASIS]

Thanks guys I appreciate it.

Agreed, I do think the regrowth was mostly from the avodart.

You are wrong my friend ,of course avodart
has a part at the temples regrowth ,
but it happened not long after I added azelaic acid.
The deteriorate at the temples occurred right after I stopped azelaic acid.

 

[IDOASIS]

Histologically, I don't believe that it has ever been shown that an improvement in scalp conditions occurs while on propecia and avodart. male pattern baldness continues while drugs like propecia and avodart cycle your hair using IGF-1 as a growth factor until the fibrosis that accompanies hair loss overwhelms even the growth stimulatory molecules that were helping you not only maintain your hair, but grow hair, as well.

I think it has been proven avodart/propecia increase haircount ,
though propecia have seen to fail in the long term.

http://www.dutasteride.org/dutasteride/ ... esults.htm

On the other hand I dont know any study which indicate avodart has
faild too.

Studies clearly show that IGF-1 is upregulated while on 5AR inhibitors.

Doctor ,
Just curios, are those studies you refer to conducted in vivo or vitro.

 

[docj077]

Histologically, I don't believe that it has ever been shown that an improvement in scalp conditions occurs while on propecia and avodart. male pattern baldness continues while drugs like propecia and avodart cycle your hair using IGF-1 as a growth factor until the fibrosis that accompanies hair loss overwhelms even the growth stimulatory molecules that were helping you not only maintain your hair, but grow hair, as well.

I think it has been proven avodart/propecia increase haircount ,
though propecia have seen to fail in the long term.

http://www.dutasteride.org/dutasteride/ ... esults.htm

On the other hand I dont know any study which indicate avodart has
faild too.

Studies clearly show that IGF-1 is upregulated while on 5AR inhibitors.

Doctor ,
Just curios, are those studies you refer to conducted in vivo or vitro.

Increasing hair count and reversing the pathophysiology of hair loss are two different things. Just because a drug makes you regrow your hair that doesn't mean that it will prevent you from going bald.

As for your last question, I believe that increases in IGF-1 have been seen both in vitro and in vivo.

 

[LookingGood!]

Thanks guys I appreciate it.

Agreed, I do think the regrowth was mostly from the avodart.

You are wrong my friend ,of course avodart
has a part at the temples regrowth ,
but it happened not long after I added azelaic acid.
The deteriorate at the temples occurred right after I stopped azelaic acid.

You cant prove that at all! There is no way you can and saying it did so is meaningless and carries no scientific proof.

 

[powersam]

ideoasis the only thing you can say with certainty is that while you were using avodart, minoxidil and azelic acid you experienced regrowth. to attribute it to the azelic acid while you are using two very potent PROVEN treatments would seem a little bit silly even when taking into account the appparent timing of the regrowth.

 

[IDOASIS]

You cant prove that at all! There is no way you can and saying it did so is meaningless and carries no scientific proof.

ideoasis the only thing you can say with certainty is that while you were using avodart, minoxidil and azelic acid you experienced regrowth. to attribute it to the azelic acid while you are using two very potent PROVEN treatments would seem a little bit silly even when taking into account the appparent timing of the regrowth.

My friends, I have said it before ,when I begun using azelaic acid I have seen a regrowth ,when I have stopped it I have seen a deteriorate.
Then I have tried it again and I have seen a regrowth again.
It is not accidental, I feel it really helped me.

 

[IDOASIS]

Increasing hair count and reversing the pathophysiology of hair loss are two different things. Just because a drug makes you regrow your hair that doesn't mean that it will prevent you from going bald.

I just dont see how is it possible ,both increasing hair count and
going bold.

I think propecia have failed in the long term becease it does not inhibit
enough scalp DHT.
I know scalp DHT is not follicie DHT ,but it is the closest data we have.

Both Serum (level circulating in the blood) Testosterone and Dihydrotestosterone were measured to evaluate Dutasteride's performance in comparison to Finasteride and placebo. The results showed that the placebo showed no inhibition, Finasteride was similar to the 0.1mg dose of Dutasteride for serum DHT inhibition (about 70%), and the higher doses of Dutasteride provided the greatest serum DHT inhibition (90% for 0.5mg and 96% for 2.5mg).

Testosterone increased 4.4% for Finasteride, 6.4% for 0.05mg Dutasteride, 16% for 0.1mg Dutasteride, and 27% for 0.5mg and 2.5mg Dutasteride. Although the rise in Testosterone may seem high, the Testosterone levels were almost always within normal range according to Rittmaster.

Scalp DHT measurements were also assessed for both DHT and Testosterone. Scalp DHT was decreased 27% for 0.05mg Dutasteride, similarly for Finasteride (38%) and Dutasteride 0.1mg (37%), 54% for 0.5mg, and 82% for 2.5mg Dutasteride. Rittmaster concluded that these results show that most of the DHT in the scalp comes from type 1 5-alpha reductase.

Scalp Testosterone rose 24% for Finasteride, 46% for 0.05mg Dutasteride, 44% for 0.1mg Dutasteride, 104% for 0.5mg Dutasteride, and 154% for 2.5mg Dutasteride.

Those results were the primary results detailed in this presentation. No results regarding efficacy or side effects were presented, other than a statement by Rittmaster that sexual side effects have occured in the studies.

As for your last question, I believe that increases in IGF-1 have been seen both in vitro and in vivo.

How many participants in the vivo study?

BTW ,Some people might not respond well to finasteride
due to a hyper-function of the androgen receptors.
Those people have shorter triplet regions of the androgen receptor gene.

http://www.hair2004.com/download/HairAb ... eil_II.pdf

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.

 

[docj077]

Increasing hair count and reversing the pathophysiology of hair loss are two different things. Just because a drug makes you regrow your hair that doesn't mean that it will prevent you from going bald.

I just dont see how is it possible ,both increasing hair count and
going bold.

I think propecia have failed in the long term becease it does not inhibit
enough scalp DHT.
I know scalp DHT is not follicie DHT ,but it is the closest data we have.

Both Serum (level circulating in the blood) Testosterone and Dihydrotestosterone were measured to evaluate Dutasteride's performance in comparison to Finasteride and placebo. The results showed that the placebo showed no inhibition, Finasteride was similar to the 0.1mg dose of Dutasteride for serum DHT inhibition (about 70%), and the higher doses of Dutasteride provided the greatest serum DHT inhibition (90% for 0.5mg and 96% for 2.5mg).

Testosterone increased 4.4% for Finasteride, 6.4% for 0.05mg Dutasteride, 16% for 0.1mg Dutasteride, and 27% for 0.5mg and 2.5mg Dutasteride. Although the rise in Testosterone may seem high, the Testosterone levels were almost always within normal range according to Rittmaster.

Scalp DHT measurements were also assessed for both DHT and Testosterone. Scalp DHT was decreased 27% for 0.05mg Dutasteride, similarly for Finasteride (38%) and Dutasteride 0.1mg (37%), 54% for 0.5mg, and 82% for 2.5mg Dutasteride. Rittmaster concluded that these results show that most of the DHT in the scalp comes from type 1 5-alpha reductase.

Scalp Testosterone rose 24% for Finasteride, 46% for 0.05mg Dutasteride, 44% for 0.1mg Dutasteride, 104% for 0.5mg Dutasteride, and 154% for 2.5mg Dutasteride.

Those results were the primary results detailed in this presentation. No results regarding efficacy or side effects were presented, other than a statement by Rittmaster that sexual side effects have occured in the studies.

As for your last question, I believe that increases in IGF-1 have been seen both in vitro and in vivo.

How many participants in the vivo study?

BTW ,Some people might not respond well to finasteride
due to a hyper-function of the androgen receptors.
Those people have shorter triplet regions of the androgen receptor gene.

http://www.hair2004.com/download/HairAb ... eil_II.pdf

[quote:3251c]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.

[/quote:3251c]

Triplet repeat mutations are not associated with hyperfunction. They are associated with loss of function. I can't think of any diseases with triplet repeat mutations that are associated with an increase in the function of any protein. Insertion of amino acids into a protein will cause it to be misfolded and force it to function poorly or not at all.

Whatever is happening with the androgen receptor is due to its inability to accomplish its physiological role...which actually isn't known. All that is known is what the physiological and anatomical consequences of a defective androgen receptor seem to be.

 

[powersam]

5ar1 is predominant in the scalp yet 5ar1 inhibitors do nothing for hair loss. 5ar2 is predominantly in the follicle and 5ar2 inhibitors have an effect on hair loss. so why does anyone still think scalp dht is important?

 

[Bryan]

My friends, I have said it before ,when I begun using azelaic acid I have seen a regrowth ,when I have stopped it I have seen a deteriorate.
Then I have tried it again and I have seen a regrowth again.
It is not accidental, I feel it really helped me.

I should point out one issue here which you appear to have overlooked: I suppose it's within the realm of possibility that azelaic acid might help fight balding by some mechanism OTHER than inhibiting 5a-reductase. You went on and on and on about that small study on azelaic acid and alopecia areata, without acknowledging that I have always been very careful to specify that what I'm talking about is whether or not azelaic acid reduces DHT. So I guess it's vaguely possible that azelaic acid is useful for male pattern baldness, but very likely not for the reason that you think.

I just dont see how is it possible ,both increasing hair count and going bold.

Losing your hair makes you BOLD? Cool!

I think propecia have failed in the long term becease it does not inhibit enough scalp DHT. I know scalp DHT is not follicie DHT ,but it is the closest data we have.

"The closest data we have"? What does THAT cryptic comment mean?

BTW ,Some people might not respond well to finasteride due to a hyper-function of the androgen receptors. Those people have shorter triplet regions of the androgen receptor gene.

You meant to say LONGER triplet regions, didn't you?

Bryan