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Hair Loss, Parts I, II, and more
- Thread starter buffdoc
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thankgodformexico
New member
Buffdoc,
I really am failing to see how there is proof lacking that dutasteride is a superior 5ar inhibitor. It has been released to treat BPH for this sole fact. If it wasn't going to outperform finasteride glaxo would not stand to gain by persuing it. It outperforms finasteride singnificantly at 3 AND 6 months, inhibiting dht at 90%.
It blocks not only BOTH enzymes, but it even dose better at blocking the type 2 than finasteride does (partly because of it's longer half life, like you have brought up.) Dht levels remain about the same around the clock on dutasteride, whereas they spike after 12hours with finasteride (leading some people to opt to take it twice daily). This is probably one of the reasons that it outperforms finasteride REGROWING HAIR, dual 5ar inhibition aside.
We still do not know if the phase 3 trials for hairloss will happen but it was put on hold for whatever reason. No one knows for sure why they did it, so to say it was because of side effects is speculative.
I don't understand why you wouldn't want to get rid of as much dht as possible when it comes to hairloss, even at the expense of a possible slight increase in sexual side effects, which can be countered other ways. Especially when in the case of many people on this board you are going to be puting synthetic testosterone into your body in mass quantity. The less coversion via 5ar the better, wouldn't you think?
I would also point out that the type 1 5ar is highly involved with sebum production in the skin/scalp, so it has potential to reduce acne as well as leave a less oily environment on the scalp preventing exsessive sebum build up which can help decrease the inflamitory process of mpb.
This is science here man, backed by studies, I'm not making any great leaps or being overly inthusiastic. Dutasteride simply IS a better 5ar antagonist, DOES regrow more hair than both finasteride and minoxidil. This is not opinion.
BTW, I'm sure you know that a handful of educated people were using finasteride by taking proscar years before it was ever in the pipeline to be marketed for hairloss as propecia. Just because a drug has only been approved by the fda to treat one ailment, does not mean that it doesn't effectively treat another ailment who's underlying mechanisms are related. Dr.'s prescribe drugs for off label use all the time, for a variety of reasons with effective results.
Please don't prevent anyone here from persuing better treatments that are scientifically backed in research to treat their hairloss. MPB is a horrid, horrid curse some of us are bestowed with and I like to see everyone get the best information possible.
I really am failing to see how there is proof lacking that dutasteride is a superior 5ar inhibitor. It has been released to treat BPH for this sole fact. If it wasn't going to outperform finasteride glaxo would not stand to gain by persuing it. It outperforms finasteride singnificantly at 3 AND 6 months, inhibiting dht at 90%.
It blocks not only BOTH enzymes, but it even dose better at blocking the type 2 than finasteride does (partly because of it's longer half life, like you have brought up.) Dht levels remain about the same around the clock on dutasteride, whereas they spike after 12hours with finasteride (leading some people to opt to take it twice daily). This is probably one of the reasons that it outperforms finasteride REGROWING HAIR, dual 5ar inhibition aside.
We still do not know if the phase 3 trials for hairloss will happen but it was put on hold for whatever reason. No one knows for sure why they did it, so to say it was because of side effects is speculative.
I don't understand why you wouldn't want to get rid of as much dht as possible when it comes to hairloss, even at the expense of a possible slight increase in sexual side effects, which can be countered other ways. Especially when in the case of many people on this board you are going to be puting synthetic testosterone into your body in mass quantity. The less coversion via 5ar the better, wouldn't you think?
I would also point out that the type 1 5ar is highly involved with sebum production in the skin/scalp, so it has potential to reduce acne as well as leave a less oily environment on the scalp preventing exsessive sebum build up which can help decrease the inflamitory process of mpb.
This is science here man, backed by studies, I'm not making any great leaps or being overly inthusiastic. Dutasteride simply IS a better 5ar antagonist, DOES regrow more hair than both finasteride and minoxidil. This is not opinion.
BTW, I'm sure you know that a handful of educated people were using finasteride by taking proscar years before it was ever in the pipeline to be marketed for hairloss as propecia. Just because a drug has only been approved by the fda to treat one ailment, does not mean that it doesn't effectively treat another ailment who's underlying mechanisms are related. Dr.'s prescribe drugs for off label use all the time, for a variety of reasons with effective results.
Please don't prevent anyone here from persuing better treatments that are scientifically backed in research to treat their hairloss. MPB is a horrid, horrid curse some of us are bestowed with and I like to see everyone get the best information possible.
Sigh...
I give up. You are failing to see my points. I don't want to deprive anyone of effective treatments. I have hair loss, too. But your reasoning is full of holes, is specious, and I'm suggesting we all become more critical in our evalulations. If you have ANY real experience in evaluating scientific studies, put it into play, with a critical eye and get back to me.
I give up. You are failing to see my points. I don't want to deprive anyone of effective treatments. I have hair loss, too. But your reasoning is full of holes, is specious, and I'm suggesting we all become more critical in our evalulations. If you have ANY real experience in evaluating scientific studies, put it into play, with a critical eye and get back to me.
thankgodformexico said:
thankgodformexico
New member
Buffdoc,
I'll just wait until they go ahead with the phase 3 trials in march of this year and hopefully the results will be clear enough for you, because the phase 2 trial obviously isn't enough.
I don't exactly know which scientific study you are referring to as far as me misinterpreting. If you'd like a can post a bunch showing dutasterides superiority to finasteride as a 5ar antagonist. I'm not really sure what you are refuting exactly, whether it IS a better 5ar antagonist, or whether it is a better drug for hairloss. The former is a black and white fact, a result from multiple double blind studies by SCIENTISTS. The latter is not solid enough for you because you don't know exactly how many subjects were in the control group and 6 months isn't an acceptable duration of time for you to draw a conclusion I guess.
I also don't see what is "scientific"about speculating about nasty side effects based on something you heard?? Where is the science in that?
This will be my last attempt to get through to you. You just keep replying with generalized statements, nothing factual, nothing scientific of your own. I am the one who has provided the trial results, and I am willing to post the rest of the studies as well. Until you can provide me with something specific, for example how I am misreading a study, which study it is, show me a study of your own with different results, or even explain to me what your point is SPECIFICLY (what I am not being critical enough about) then this is useless. PLease enlighten me.
I'll just wait until they go ahead with the phase 3 trials in march of this year and hopefully the results will be clear enough for you, because the phase 2 trial obviously isn't enough.
I don't exactly know which scientific study you are referring to as far as me misinterpreting. If you'd like a can post a bunch showing dutasterides superiority to finasteride as a 5ar antagonist. I'm not really sure what you are refuting exactly, whether it IS a better 5ar antagonist, or whether it is a better drug for hairloss. The former is a black and white fact, a result from multiple double blind studies by SCIENTISTS. The latter is not solid enough for you because you don't know exactly how many subjects were in the control group and 6 months isn't an acceptable duration of time for you to draw a conclusion I guess.
I also don't see what is "scientific"about speculating about nasty side effects based on something you heard?? Where is the science in that?
This will be my last attempt to get through to you. You just keep replying with generalized statements, nothing factual, nothing scientific of your own. I am the one who has provided the trial results, and I am willing to post the rest of the studies as well. Until you can provide me with something specific, for example how I am misreading a study, which study it is, show me a study of your own with different results, or even explain to me what your point is SPECIFICLY (what I am not being critical enough about) then this is useless. PLease enlighten me.
thankgodformexico said:
Your arrogance is impressive. Now, where is your degree from and in what?
I don't need to be "gotten though" to. We are obviously not communicating from anywhere near the same knowledge base. There is a difference between simply reading studies off the internet and buying into the conclusions the drug companies make, and in having a more in-depth understanding of the workings of clinical and basic science research, as well as the requirements for staistical significance and what that means. Do you possess that awareness?
I have not said that dut is not a superior 5-AR inhibitor than fin. What I HAVE said is that this does not necessarily translate to long-term, improved clinical results. We simply don't have the data to show that. If you even understood the research process, then we wouldn't be having this discussion. This is not about what studies you "have" or I need to "show" you; it's about your less than complete understanding about how we INTERPRET said studies.
Also, your naive idea that a drug company such as Glaxo would only release a drug, dutasteride for example, if it were definitely superior to it's competition, is laughable. Every month, new drugs are released soley for the purpose of grabbing a piece of market share. Pursuit of FDA approval does NOT necessarily imply a superior product in any way, shape or form.
Again, I'm not here to attack your beloved dutasteride (it may turn out to be great, and I'll definitely prescribe it and use it personally, if that be the case). Nor am I here to tell you "your" studies are flawed; just that you don't seem
to have even the basic graduate student's grasp of the interpretation of scientific data. I can't be any more "specific" than that, because the problem is a general one on your part.
thankgodformexico
New member
I'm not trying to be arrogant at all.
"I have not said that dut is not a superior 5-AR inhibitor than fin. What I HAVE said is that this does not necessarily translate to long-term, improved clinical results. We simply don't have the data to show that."
That's all I was trying to get from you, and you are 100% right. We don't have long term data on dutasteride so we don't know how it will do in the long run, but then again the 5 year finast results were released not too long ago and people have been using it from the get go.
I understand that there is a definite limit on the success of anti-androgens to treat hairloss. Even castrated males do not regrow any hair although the mpb process ceases. I don't claim to be a doctor or a scientist at all, just trying to contribute something that might be a hopeful new treatment for mpb (even if it is only slightly better).
IMO I would rather spend less money on dutasteride than proscar and have the extra comfort of knowing that I am eliminating as much dht as I possibly can. I was just having a hard time understanding your sceptisism and trying to see why you felt that way. Assuming that the side effects aren't marginally higher than finasteride, will you try it yourself or prescribe it for your patients? You could do your own personal trial and draw a first hand conclusion. What is there to lose?
"I have not said that dut is not a superior 5-AR inhibitor than fin. What I HAVE said is that this does not necessarily translate to long-term, improved clinical results. We simply don't have the data to show that."
That's all I was trying to get from you, and you are 100% right. We don't have long term data on dutasteride so we don't know how it will do in the long run, but then again the 5 year finast results were released not too long ago and people have been using it from the get go.
I understand that there is a definite limit on the success of anti-androgens to treat hairloss. Even castrated males do not regrow any hair although the mpb process ceases. I don't claim to be a doctor or a scientist at all, just trying to contribute something that might be a hopeful new treatment for mpb (even if it is only slightly better).
IMO I would rather spend less money on dutasteride than proscar and have the extra comfort of knowing that I am eliminating as much dht as I possibly can. I was just having a hard time understanding your sceptisism and trying to see why you felt that way. Assuming that the side effects aren't marginally higher than finasteride, will you try it yourself or prescribe it for your patients? You could do your own personal trial and draw a first hand conclusion. What is there to lose?
Anyone know of other internet sites to obtain Avodart?
Since its obviously not a scheduled substance I was wondering if there were any other websites anyone had come across to order Avodart from w/o the "internet consultation fee". For a long time I have ordered my ancillary meds from sites such as MedsMex which does not have this extra fee, but sadly they do not currently offer Avodart. Even if dutesteride is unproven in the long term I for one would be willing to try it. If the main side effect is a depressed sex drive I'm sure its not as acute as doing a fina only cycle, and even if it is so be it. Its much easier to study when not obsessing on female ass all the time.
Since its obviously not a scheduled substance I was wondering if there were any other websites anyone had come across to order Avodart from w/o the "internet consultation fee". For a long time I have ordered my ancillary meds from sites such as MedsMex which does not have this extra fee, but sadly they do not currently offer Avodart. Even if dutesteride is unproven in the long term I for one would be willing to try it. If the main side effect is a depressed sex drive I'm sure its not as acute as doing a fina only cycle, and even if it is so be it. Its much easier to study when not obsessing on female ass all the time.
IMO I would rather spend less money on dutasteride than proscar and have the extra comfort of knowing that I am eliminating as much dht as I possibly can. I was just having a hard time understanding your sceptisism and trying to see why you felt that way. Assuming that the side effects aren't marginally higher than finasteride, will you try it yourself or prescribe it for your patients? You could do your own personal trial and draw a first hand conclusion. What is there to lose? [/B][/QUOTE]
That's a thought, but I don't know. I'm still a little leary of the long half life, maybe that's just my personal paranoia.
As to eliminating as much DHT as possible, another thing I'm interested to know is if either of these 5-AR inhibitors can really do the job (or at least keep DHT levels w/in normal limits) when people are using AAS, and have supraphysiologic levels. If not, then those who juice would seem to be at the mercy of their own genetics.
What do you think?
That's a thought, but I don't know. I'm still a little leary of the long half life, maybe that's just my personal paranoia.
As to eliminating as much DHT as possible, another thing I'm interested to know is if either of these 5-AR inhibitors can really do the job (or at least keep DHT levels w/in normal limits) when people are using AAS, and have supraphysiologic levels. If not, then those who juice would seem to be at the mercy of their own genetics.
What do you think?
thankgodformexico
New member
"That's a thought, but I don't know. I'm still a little leary of the long half life, maybe that's just my personal paranoia.
I'm guessing and others have speculated that the long half life might be one of the reasons it performs better than finast (at least according to glaxo's phase 2 trial), dht levels spike a bit after 12 hours with finast where dut keeps them consistantly lower around the clock.
"As to eliminating as much DHT as possible, another thing I'm interested to know is if either of these 5-AR inhibitors can really do the job (or at least keep DHT levels w/in normal limits) when people are using AAS, and have supraphysiologic levels. If not, then those who juice would seem to be at the mercy of their own genetics.
What do you think?"
This is the million dollar question, and I have no idea. Your guess would be better than mine. I think it would be awsome if either drug was able to keep dht within the norm while on a cycle, but I have a gut feeling that they probably just help dampen the blow some. I'm in early week 3 of a 500mg test/400mg deca cycle and I am starting to notice that tell-tale itching that is indicative of thr notorious mpb (at least in my case).
I tried to guess at this a while ago using what is probably errored logic but I was wondering if you could figure it out like this. Taking the normal daily natural amount of test production by the body which I believe is around 5-7mg...figuring that finasteride reduces around 70% dht...then just subtracting 70% of the 5-7mg to get a hypothetical amount of dht in mg (the left over 30%)that would be left to circulate (not even accounting for any test to est conversion via aromatase). Then take 500mg test which I am on weekly, divide by 7 (days in the week), get a daily amount in mg and do the same thing to get a figure in mg. I'm sure this method is highly flawed, but just for the hell of it...by this method you get like 2.1mg left over dht by the body without added test, as opposed to around 21mg with the added 500mg test. This was the only way I could figure to even just guess at comparing the two and I have no idea if you can even calculate it this way.
I'm guessing and others have speculated that the long half life might be one of the reasons it performs better than finast (at least according to glaxo's phase 2 trial), dht levels spike a bit after 12 hours with finast where dut keeps them consistantly lower around the clock.
"As to eliminating as much DHT as possible, another thing I'm interested to know is if either of these 5-AR inhibitors can really do the job (or at least keep DHT levels w/in normal limits) when people are using AAS, and have supraphysiologic levels. If not, then those who juice would seem to be at the mercy of their own genetics.
What do you think?"
This is the million dollar question, and I have no idea. Your guess would be better than mine. I think it would be awsome if either drug was able to keep dht within the norm while on a cycle, but I have a gut feeling that they probably just help dampen the blow some. I'm in early week 3 of a 500mg test/400mg deca cycle and I am starting to notice that tell-tale itching that is indicative of thr notorious mpb (at least in my case).
I tried to guess at this a while ago using what is probably errored logic but I was wondering if you could figure it out like this. Taking the normal daily natural amount of test production by the body which I believe is around 5-7mg...figuring that finasteride reduces around 70% dht...then just subtracting 70% of the 5-7mg to get a hypothetical amount of dht in mg (the left over 30%)that would be left to circulate (not even accounting for any test to est conversion via aromatase). Then take 500mg test which I am on weekly, divide by 7 (days in the week), get a daily amount in mg and do the same thing to get a figure in mg. I'm sure this method is highly flawed, but just for the hell of it...by this method you get like 2.1mg left over dht by the body without added test, as opposed to around 21mg with the added 500mg test. This was the only way I could figure to even just guess at comparing the two and I have no idea if you can even calculate it this way.
Most of what I have read regarding saw palmetto inidcates that its 5-ar inhibition properties are very low to non-existant at typical dosages. SP is extraordinarily effective at relieving symptoms of BPH, whether androgen induced or not. This quality seems to be the result of some pathway other than androgen receptor. It also lowers PSA levels significantly after several days of administration. As you are most likely aware, there are no conclusive studies definatively linking one's PSA level to suceptibility of prostate cancer. This substance is the preferred course of treatment over finasteride for BPH in europe.
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