I don’t care if you have been here longer than me, since that doesn’t change the fact that oral minoxidil inhibits collagen.
If Hairloss Is All About Dht Level...
- Thread starter NiBBa
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I don’t care if you have been here longer than me, since that doesn’t change the fact that oral minoxidil inhibits collagen.
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That’s nice, should be tons of testimonials that would confirm this fact right?
I can confirm that Obsessive had issues with oral minoxidil causing giant veins on his arms, and that Georgie has signs of bad skin from oral minoxidil. Although, I would love to see the condition of your skin!
Thanks i am thinking of doing ru58841 in alfatradiol solution, thoughts? I have high T and high DHT so ru should technically block both..
thoughts on RU58841 to block androgens on scalp?I can confirm that Obsessive had issues with oral minoxidil causing giant veins on his arms, and that Georgie has signs of bad skin from oral minoxidil. Although, I would love to see the condition of your skin!
I think RU is one of the worst remedies for hair loss
looking for an alternative to finasteride/dutasteride. They skyrocket my T to like 1300 and my balls hurt. That's a 50-60% increase in T> i am taking finasteride now but long term can't be good..
maybe CB0301?
Have there been much success stories on that?
That’s quite common, unfortunately... My T is around 136 ng/dL...
I recently had my hormones checked, since I asked my endocrinologist for a blood test. My FSH is significantly reduced, along with my T. My E is above the aimed levels for transgender women, and my LH is within normal levels for a male.
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LoL avg hormone levels of reddit poster
What?
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Loss of collagen due to aging is a big factor.
https://www.beIgraviacentre.com/blog/japanese-researchers-link-age-related-hair-loss-to-collagen/
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I noticed diffuse thinning and recession in my early 20’s. I don’t know if it is a myth but I have read several times that by the time you can visually notice thinning, you have lost at least 50% of your hair in that area. Keep in mind we have thousands of hair follicles.
But it makes me wonder that if I noticed at 21 and that meant it was a 50% loss in those areas, then when did the loss actually start?! 16? 17? Odd.
I have maintained with RU.
I did finasteride for a year in my mid 20’s and it did help some but the sides were terrible. Gyno, acne etc. I tried dutasteride for a month and that was worse, obviously. Same sides just more severe. Both went away when I stopped finasteride and later dutasteride.
But it makes me wonder that if I noticed at 21 and that meant it was a 50% loss in those areas, then when did the loss actually start?! 16? 17? Odd.
I have maintained with RU.
I did finasteride for a year in my mid 20’s and it did help some but the sides were terrible. Gyno, acne etc. I tried dutasteride for a month and that was worse, obviously. Same sides just more severe. Both went away when I stopped finasteride and later dutasteride.
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What's the problem with RU ? Blocking the receptors sounds like the way to go, instead of systemically blocking one of the most potent androgens in your body.
persistentone
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Why?
DoctorHouse
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This was posted on another forum by Dr Cole but I think he explains what happens:
Hair loss goes in plateaus. You stabilize and then you drop off the cliff typically. Then you land on another plateau, which you usually fall off of later on. DHT blockers do slow down the aging process. However, they do not work equally well in all individuals. Furthermore, DHT blockers alone are not the sole answer most likely. The hair loss process is quite complex. If DHT alone were the culprit, then all would respond with a full head of hair with dutasteride, which blocks most of the DHT. There are multiple pathways involved in the cell cycling process. Every cell has a limited number of cycles. Once a cell reaches the maximum number of cycles, stem cell populations are lost and the cell cannot replicate. In the hair follicle, there is an interaction between the secondary hair germ, which gives rise to the inner root sheath and the matrix, and the hair follicle stem cells of the bulge. BMP keeps the hair follilce in the resting, telogen phase. BMP suppression by noggin, produced by the secondary hair germ, causes the dermal papilla to turn off BMP expression and thus, upregulates Wnt/B-catenin from the bulge stem cells and induces the growing phase and gives rise to the outer root sheath. There are all kinds of BMP and WNT. Furthermore, there is Notch signaling is a downstream pathway can turn off anagen.
Because cells have a limited number of cycles, the goal is to keep the hair follicle in anagen as long as possible. In androgenic alopecia, the percentage of follicles in the resting telogen phase is markedly increased. We want to keep these follicles in the active growing phase as long as possible so that they can have the longest possible life span. One does not want to start anti-aging medicine once you are old. You start when you are young. Once the stem cell niche is lost, there is no way to bring that follilce back at this time. This is why it is so important to attack hair loss from multiple pathways. DHT is only a single consideration. I have followed enough patients over 20 to 30 years to see what happens to them. They all lose hair, often to the point that hair restoration is no longer an option. In fact, it may prove to be a bad idea to begin with. For this reason, I am a very strong proponent of all newer modalities to improve the life span of the hair follicle. I am even more ardently supportive of maintaining the hair follicle as long as possible than I am of hair restoration surgery.
Maintaining hair follicles is essential. Once you go beyond a Norwood 3V there is no hope you will ever get a full head of hair through transplantation using traditional methods alone. Thus, it is up to the individual patient to seek all potential modalities to maintain their hair as long as possible. I am hopeful that exosomes alone will be the single best option to effect this change in the life cycle alone. This is why I am offering exosome treatment in New York, among other locations at this time. I believe we will find that exosomes the key ingredient in all anti-aging modalities including PRP, CRP, amniotic membrane, and adipose stem cells (stromal vascular fraction). But time will tell. It could be that a combination of adipose stem cells and exosomes is the best treatment. What I can tell you is that amniotic membrane has a stronger influence on dermal papilla proliferation than PRP or CRP.
Don't get too comfortable with a single treatment nor that you will never lose more hair.
Hair loss goes in plateaus. You stabilize and then you drop off the cliff typically. Then you land on another plateau, which you usually fall off of later on. DHT blockers do slow down the aging process. However, they do not work equally well in all individuals. Furthermore, DHT blockers alone are not the sole answer most likely. The hair loss process is quite complex. If DHT alone were the culprit, then all would respond with a full head of hair with dutasteride, which blocks most of the DHT. There are multiple pathways involved in the cell cycling process. Every cell has a limited number of cycles. Once a cell reaches the maximum number of cycles, stem cell populations are lost and the cell cannot replicate. In the hair follicle, there is an interaction between the secondary hair germ, which gives rise to the inner root sheath and the matrix, and the hair follicle stem cells of the bulge. BMP keeps the hair follilce in the resting, telogen phase. BMP suppression by noggin, produced by the secondary hair germ, causes the dermal papilla to turn off BMP expression and thus, upregulates Wnt/B-catenin from the bulge stem cells and induces the growing phase and gives rise to the outer root sheath. There are all kinds of BMP and WNT. Furthermore, there is Notch signaling is a downstream pathway can turn off anagen.
Because cells have a limited number of cycles, the goal is to keep the hair follicle in anagen as long as possible. In androgenic alopecia, the percentage of follicles in the resting telogen phase is markedly increased. We want to keep these follicles in the active growing phase as long as possible so that they can have the longest possible life span. One does not want to start anti-aging medicine once you are old. You start when you are young. Once the stem cell niche is lost, there is no way to bring that follilce back at this time. This is why it is so important to attack hair loss from multiple pathways. DHT is only a single consideration. I have followed enough patients over 20 to 30 years to see what happens to them. They all lose hair, often to the point that hair restoration is no longer an option. In fact, it may prove to be a bad idea to begin with. For this reason, I am a very strong proponent of all newer modalities to improve the life span of the hair follicle. I am even more ardently supportive of maintaining the hair follicle as long as possible than I am of hair restoration surgery.
Maintaining hair follicles is essential. Once you go beyond a Norwood 3V there is no hope you will ever get a full head of hair through transplantation using traditional methods alone. Thus, it is up to the individual patient to seek all potential modalities to maintain their hair as long as possible. I am hopeful that exosomes alone will be the single best option to effect this change in the life cycle alone. This is why I am offering exosome treatment in New York, among other locations at this time. I believe we will find that exosomes the key ingredient in all anti-aging modalities including PRP, CRP, amniotic membrane, and adipose stem cells (stromal vascular fraction). But time will tell. It could be that a combination of adipose stem cells and exosomes is the best treatment. What I can tell you is that amniotic membrane has a stronger influence on dermal papilla proliferation than PRP or CRP.
Don't get too comfortable with a single treatment nor that you will never lose more hair.