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Originally Posted by burtandernie
I dont think some people understand the concept of what a drug really is. If your on finasteride which is approved for MPB and easily the most effective thing why would you consider using dutasteride too without even seeing how the first thing works? I would read a little about what DHT actually does before you touch dut.
Studies make it seem like dut is more effective than fin. Also these drugs do not suppress DHT completely. tbh DHT is not a big concern after puberty, it is a crap hormone that makes your hair disappear. The only concerns should be about other functions of 5-ar enzymes & also other hormones becoming unbalanced (estrogen, T etc)
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I would love to understand what people mean by genotypes responding better or worse to fin or dut. This could help us determine which drug to choose.
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Originally Posted by Assemblage23
I would love to understand what people mean by genotypes responding better or worse to fin or dut. This could help us determine which drug to choose.
Yes me too. Reading about this on forums is part of the reason I take both
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dutas + finast
I have been taking both for a couple years now. Also 1mg of dut and 5mg fin..no real side effects to speak of. I started this because finasteride didn't give me great results and dutasteride I was only giving me marginal results so I decided to use both and the results have been quite good..
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Heres a study...Shows comparison of inhibition in different genotypes between fin and dut.
http://jme.endocrinology-journals.or.../34/3/617.long
For the most part dut is superior but there are exceptions
eg.
''However, two of the enzyme variants do not follow this trend: the F194L variant (independently of reaction time) and the P48R variant (but only in the 10-min reaction) display lower apparent Ki (higher affinity) for finasteride than dutasteride (Tables 1⇑ and 2⇑).''
Blood tests are crucial. You could waste years taking fin when it is doing nothing for you, or years taking dut when you should be on fin.
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Originally Posted by Dan26
Heres a study...Shows comparison of inhibition in different genotypes between fin and dut.
http://jme.endocrinology-journals.or.../34/3/617.long
For the most part dut is superior but there are exceptions
eg.
''However, two of the enzyme variants do not follow this trend: the F194L variant (independently of reaction time) and the P48R variant (but only in the 10-min reaction) display lower apparent Ki (higher affinity) for finasteride than dutasteride (Tables 1⇑ and 2⇑).''
Blood tests are crucial. You could waste years taking fin when it is doing nothing for you, or years taking dut when you should be on fin.
So can a doctor determine if fin or dut is working simply by taking blood tests? If so, how often would one be getting the tests?
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Im a chemist and the short to whether a doctor can tell one drug is better for you than the other is No. It would require scalp samples and would go beyond the cost and know how that an average doctor could do. these are the things that go into a study and not the average practice of a general practitioner.even though I am new here I have worked on 5 alpha reductase inhibitors for over 15 years and its a very complicated issue. For example, dutasteride should stop all skin oil sebum for those in the know but it doesn't which postulates that there is more to 5 alpha reductase inhibitors then currently known. Dutaseride should stop acne ala accutane through inhibition of sebum but it doesnt. what I'm saying is that we have a lot more to learn and so does any doctor. dutasteride should cure male pattern baldness but its only A somewhat effective treatment, combined with finasteride even better. Blood tests don't measure scalp dht or dyhydroepiandosterone which is thought to be another culprit.
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Blood tests will tell you if your serum DHT is being lowered, so they are crucial. Just because serum DHT is lowered does not necessarily mean the drugs will work, but it means that you respond as far as 5ar2 inhibition goes. If your serum DHT is not lowered it is likely you are not responding to the drug as most do ie your 5ar2 is not being sufficiently inhibited, and one reason this may be so is due to your genotype.
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The problem with all this stuff like fin or dut is they always look at something like DHT just in isolation of all the other stuff going on and its all interconnected. You cant just look at DHT without looking at testosterone or what about the most important issue of why is hair sensitive to androgens? How do androgen receptors react with lowering DHT over time? Lots of questions besides just lowering DHT that all affect how something like propecia works.
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Originally Posted by burtandernie
The problem with all this stuff like fin or dut is they always look at something like DHT just in isolation of all the other stuff going on and its all interconnected. You cant just look at DHT without looking at testosterone or what about the most important issue of why is hair sensitive to androgens? How do androgen receptors react with lowering DHT over time? Lots of questions besides just lowering DHT that all affect how something like propecia works.
Yes this is true there is a feedback system in your body ie homeostasis that causes inevitable chain reactions (which is why i never beleived in that keratene alpha retard stuff which claimed to lower DHT with no changes in other androgenic hormones)...again, bloodtests are very important when on fin and dut. Oddly LH hormone is actually raised on dut unlike on fin which helps explain why sexual dysfuntion seems less prevalent with dut (but ofcourse higher risk of mental sides and estrogenic sides)
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