Thanks for replying
and YES! this is my concern. If that is true, why did the doctors say
"Dutasteride at high doses in some trials appears better than finasteride. But that's not the doses we presribe!" Are they nuts?
Yes, they appear to be nuts (or at least, very misinformed). Dutasteride at a tiny dose of 0.1mg inhibits approximately the same amount of DHT as 5mg of Finasteride does. Dutasteride is a much more potent DHT inhibitor than Finasteride.
Good accurate stuff. But in the medical literature there was one patient who was on 1 mg finasteride per day for 4 years, first his crown improved a bit, but 2 years later the effects wore off and he was almost back to baseline. He simply added just ONE 0.5 mg dutasteride pill per week with the daily finasteride and in 3 months it did more than finasteride ever did.
Maybe it's not just about DHT, maybe some genotypes will respond better to dutasteride/finasteride.
Almost all 5ar genotypes respond better to dutasteride than finasteride. Take a look at this study:
http://jme.endocrinology-journals.org/content/34/3/617.full
This paragraph was interesting:
"
Comparison of the apparent K[SUB]i[/SUB] values for each inhibitor suggests that dutasteride was the steroid 5α-reductase inhibitor that exhibited the lowest apparent K[SUB]i[/SUB] for most steroid 5α-reductase variants, including the wild-type, in both the 10-min and the 30-min reactions (Tables 1 and 2). The only exceptions to this observation were the F194 L variant (independently of reaction time) and the P48R variant (but only in the 10-min reaction). The disease-relevant A49T variant is of particular interest, since it is inhibited much more efficiently by dutasteride than finasteride, irrespective of the reaction time (Tables 1 and 2). Overall, the dual 5α-reductase inhibitor, dutasteride, has higher affinity for steroid 5α-reductase type II than finasteride, irrespective of genotype. Dutasteride is also expected to result in lower pharmacogenetic variation than finasteride in vivo, since it displays significantly lower pharmacogenetic variation of the apparent K[SUB]i[/SUB] than finasteride in the 30-min assays (see below; Tables 1 and 2). Thus, this compound may also be a better choice in vivo."
Interestingly, the F194L variant was found to be inhibited more potently by Finasteride than Dutasteride in both the 10-min and the 30-min reactions. A person with this genotype, therefore, would presumably get better results from using finasteride rather than dutasteride to treat their hair loss.
I do have some knowledge of genetics, and I know that we each have two copies of each of our genes. Therefore, we have two copies of the 5-ar type 2 gene. I think it is most likely the case that both these copies would need to be the F194L allele in order for finasteride to work better for you than dutasteride, rather than just one of the two copies being the F194L variant. I'm guessing that the likelihood of this variant occurring in the homozygous (two copies) state is very uncommon.
I think it's more because the two drugs have different mechanisms and can work in synergy. The guy was taking finasteride, which lowered his DHT by 70%, and the simple addition of 0.5mg of dutasteride a week took care of the remaining 30%.
I doubt that the two drugs operate in the way you have described. Adding 0.5mg of dutasteride a week to a finasteride regimen might bring down your DHT slightly more than if you were just using the finasteride, but it wouldn't make a big difference.
If you're using finasteride and dutasteride together, whichever one is weaker (depending on the dosage and your genotype) will be overpowered by the stronger one, and you will get no more DHT inhibition than if you were just using the stronger inhibitor alone.
