We've seen 1 year results of proscar, and also a 17 identical twin study with dutasteride 0.5mg, with the other twin being placebo. In both cases, the 6 month results of other studies were duplicated, but the 1 year results showed numbers similar to propecia's 1 year results. This makes some of us wonder if higher DHT inhibition just gives faster results, and not better results.
However, dutasteride 2.5mg climbed higher above baseline at 6 months than propecia did by 1 or 2 years, by a good margin. I think I know why:
I've been thinking about how androgens seem to permenantly kill head hair and permenantly lengthen body hair, but I think estrogen can reverse it, but we just can't use it unfortunately. I believe this because I heard that female hair loss, unlike male hair loss, is not permenant. Women respond better to 2% minoxidil than men do to 5%.
Back to the 2.5mg:
The DHT from 5ar2 in the follicle is the most important damage to the follicle. I think at least half if not 2/3 of the testosterone in the follicle is turned to DHT. So when that testosterone is prevented from turning to DHT, it is able to be turned to estrogen, which is good. (BTW, greatly fluctuating extrogen levels cause hair to shed, so I think it is good to minimize fluctuation) Anyway, finasteride and lower dutasteride all suppress scalp DHT about the same: 40-50%. So the estrogen levels are about the same. Also, whether 90% or 98.5% of DHT is inhibited does not seem to make a huge difference, especially when even testosterone can do a little damage.
OK, here is the kicker: dutasteride 2.5mg suppressed 85% of 5ar1, the most prominent DHT making in the scalp. That must free up a lot more testosterone in the scalp to be made to estrogen, as well as reducing local DHT levels. Also, the estrogen levels are probably more stable.
Now I don't want to inhibit 85% of the DHT in my nerve cells. But topical white curcumin, or topical free fatty acids (revivogen) can do the job locally. I recommend applying them opposite your finasteride dose.
spironolactone and RU: good at reducing androgen activity, but do they also bind to the estrogen receptor? Not good. We need that estrogen receptor active, but don't want DHT binding to it. Rather than worry about testosterone binding to the androgen receptor, I'd rather apply anti-oxidants to negate the chemicals testosterone produces. So no RU or spironolactone for me once my white curcumin arrives. I will apply spironolactone to my body hair though. Thinking about it.
I definitely want to even out my oral 5ar dose, so my estrogen levels stay more constant. Good news: any hair shed by estrogen fluctuation is not permenantly lost. It just went into tellogen early and will be back. But higher scalp estrogen is good.
However, dutasteride 2.5mg climbed higher above baseline at 6 months than propecia did by 1 or 2 years, by a good margin. I think I know why:
I've been thinking about how androgens seem to permenantly kill head hair and permenantly lengthen body hair, but I think estrogen can reverse it, but we just can't use it unfortunately. I believe this because I heard that female hair loss, unlike male hair loss, is not permenant. Women respond better to 2% minoxidil than men do to 5%.
Back to the 2.5mg:
The DHT from 5ar2 in the follicle is the most important damage to the follicle. I think at least half if not 2/3 of the testosterone in the follicle is turned to DHT. So when that testosterone is prevented from turning to DHT, it is able to be turned to estrogen, which is good. (BTW, greatly fluctuating extrogen levels cause hair to shed, so I think it is good to minimize fluctuation) Anyway, finasteride and lower dutasteride all suppress scalp DHT about the same: 40-50%. So the estrogen levels are about the same. Also, whether 90% or 98.5% of DHT is inhibited does not seem to make a huge difference, especially when even testosterone can do a little damage.
OK, here is the kicker: dutasteride 2.5mg suppressed 85% of 5ar1, the most prominent DHT making in the scalp. That must free up a lot more testosterone in the scalp to be made to estrogen, as well as reducing local DHT levels. Also, the estrogen levels are probably more stable.
Now I don't want to inhibit 85% of the DHT in my nerve cells. But topical white curcumin, or topical free fatty acids (revivogen) can do the job locally. I recommend applying them opposite your finasteride dose.
spironolactone and RU: good at reducing androgen activity, but do they also bind to the estrogen receptor? Not good. We need that estrogen receptor active, but don't want DHT binding to it. Rather than worry about testosterone binding to the androgen receptor, I'd rather apply anti-oxidants to negate the chemicals testosterone produces. So no RU or spironolactone for me once my white curcumin arrives. I will apply spironolactone to my body hair though. Thinking about it.
I definitely want to even out my oral 5ar dose, so my estrogen levels stay more constant. Good news: any hair shed by estrogen fluctuation is not permenantly lost. It just went into tellogen early and will be back. But higher scalp estrogen is good.