curiosity
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I am not a doctor that treats hair loss. This is all just theory:
Steroidal 5 alpha-reductases (finasteride and dutasteride) bother me because their binding is irreversible. I worry that this ultimately changes the androgen receptor concentrations at the level of the follicle to make them hypersensitive to DHT, thus making your hair fall out more easily in the long run. This appears to be what happens with prostate cancers that learn resistance to hormonal chemotherapy.
There are many herbal nonsteroidal inhibitors, but I have heard mixed reviews here. There are also some pharmaceutical ones (LY191704, FK143), but I need to do more reading.
What are everyone's thoughts on this subject?
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One counter argument that I can think of is that in prostate cancer, you have a cell that is uncontrollably dividing. The drive for mitosis is what spawns natural selection principles of resistance to hormonal stimuli. With hair follicles, you have exactly the opposite -- they're dying, not dividing.
You're artificially keeping alive hair that would be dead otherwise. Of course you will be left with is hair that is resistant to your medication. That does not necessarily mean it will be sensitive to the low levels of DHT you create with your medication. And, it could be argued that all you will be left with is hair that is sensitive to your medication.
But I do still think chronically low levels of DHT created by irreversible covalent bonds have the potential to change end organ (read: hair follicle) tissue receptors, and that is concerning to me.
Steroidal 5 alpha-reductases (finasteride and dutasteride) bother me because their binding is irreversible. I worry that this ultimately changes the androgen receptor concentrations at the level of the follicle to make them hypersensitive to DHT, thus making your hair fall out more easily in the long run. This appears to be what happens with prostate cancers that learn resistance to hormonal chemotherapy.
There are many herbal nonsteroidal inhibitors, but I have heard mixed reviews here. There are also some pharmaceutical ones (LY191704, FK143), but I need to do more reading.
What are everyone's thoughts on this subject?
- - - Updated - - -
One counter argument that I can think of is that in prostate cancer, you have a cell that is uncontrollably dividing. The drive for mitosis is what spawns natural selection principles of resistance to hormonal stimuli. With hair follicles, you have exactly the opposite -- they're dying, not dividing.
You're artificially keeping alive hair that would be dead otherwise. Of course you will be left with is hair that is resistant to your medication. That does not necessarily mean it will be sensitive to the low levels of DHT you create with your medication. And, it could be argued that all you will be left with is hair that is sensitive to your medication.
But I do still think chronically low levels of DHT created by irreversible covalent bonds have the potential to change end organ (read: hair follicle) tissue receptors, and that is concerning to me.