Finasteride didn't work for you? So, did DUT?

[BaldingHelpMe]

DUT takes a long time to reach a steady state, but once it does youre DHT levels will pretty much remain at their lowest levels.

It takes three months for dut to get to your body?? Says who? Where did you get this info? Also, it doesn't make sense. From the leaflet, it says the medicine will get to your bloodstream in a few hours after taking it.

[dm90]

I said it takes three months to reach a "steady state". A steady state is a term used in pharmacokinetics where the drug is ingested at the same rate it is removed, this means the concentration remains steady in your blood. This is why people talk about "loading doses" with avodart.

[tedwuji]

I said it takes three months to reach a "steady state". A steady state is a term used in pharmacokinetics where the drug is ingested at the same rate it is removed, this means the concentration remains steady in your blood. This is why people talk about "loading doses" with avodart.

It crosses blood brain barrier which is not relevant to an obession with maximizing the reduction of androgens but castration side-effect is also irrelevant under parallel logic.

[tedwuji]

They're different animals, but completely pointless distinctions. They are also are irrelevant to fin/dut effectives in treating hairloss. The 98% figure i stated was dermal papilla type 2 dht, which as far as we know is the only relevant DHT with regards to hairloss, remember its an autocrine response not paracrine. Serum DHT is just the DHT concentration in the entire body, which includes scalp DHT. Yes most are well versed in the reduction percent curve of finasteride, approx 70% serum, and dutasteride approx 90%. But You have to understand what these numbers mean. Why can serum dht be reduced by 90% while scalp dht is only reduced by 50%? Because DHT isnt evenly concentrated throughout the body. Type 2 is heavily concentrated in the prostate and dermal papilla while type 1 is present in the sebaceous glands and brain. Neither have any significant concentration in the skeletal muscle. Sebaceous glands are in the scalp and therefore there is a significant concentration of the type 1 isoform. Finasteride has no affinity for this isoform and dutasteride, while it does reduce it, doesnt have nearly as strong of an affinity for it as it does for the type 2. Secondly and the most important point is the ratio of type 1 to type 2 in the body. The majority of DHT in the body is converted from the type 2 isoenzyme. I approximately 70-80% of total dht actually. Firstly FIN reduces total serum dht by 70%. Secondly FIN has no affinity for the type 1 isoenzyme, therefore that 70% reduction is completely type 2. Well 70 is about 90% of 80. So given the perfect response finasteride reduces type 2 dht by 90%. This means there is only 10% DHT left in the dermal papilla, the only important DHT. DUT has 3x affinity for the type 2 isoenzyme over finasteride, this means significantly more type 2 is reduced leaving next to no traces of the hormone in the follicle. Lastly, yes type 1 is present in the brain tissue, and dutasteride can pass the blood brain barrier. That isnt really relevant to the point im making.

It crosses blood brain barrier which is not relevant to an obession with maximizing the reduction of androgens but castration side-effect is also irrelevant under parallel logic.

[dm90]

It crosses blood brain barrier which is not relevant to an obession with maximizing the reduction of androgens but castration side-effect is also irrelevant under parallel logic.

I don't quite understand the statement here. I wasn't arguing the safety long term safety of dutasteride, nor was I advocating its use. I was simply comparing the pharmokinetics of the drug to finasteride and offering an explanation as to why dut will work when finasteride fails. As for the blood brain barrier, several medications cross it, finasteride does however the type 2 enzyme doesnt appear to be present in brain tissue. As for the reduction statement I made that seemed to provide some confusion here is a study to confirm what I have said. http://onlinelibrary.wiley.com/doi/1...06.00053.x/pdf

"However, finasteride decreases prostatic DHT concentrations
(where the Type II enzyme predominates) by as much as 90%"

However there is a standard deviation by about 20% leaving some to only have around a 60% reduction in type 2. Dutasteride has 3x the affinity for the type II isoform and a much lower SD. The original question for this thread is asking if DUT will succeed when fin has failed, and the answer to that question is it more than likely will.

I'm not here to argue the safety profile of a drug or persuade someone to take anything. Sertraline crosses the blood brain barrier, it has to in order to work, and its rate of sexual side effects are much higher than and A5RI, some studies have shown the rates are as high as 30-40%. Also persistent sexual dysfunction is well documented for this medication, however the same paranoia doesnt seem to surround SSRI's possibly because depression, ocd, and anxiety are taken much more seriously while hairloss is considered an issue of vanity. I'm not demonizing SSRI's either, I believe they help alot of people who desperately need it. Some are completely emotionally crippled by hairloss and finasteride doesnt work for everyone. People need an objective understanding of available treatments so they can decide for themselves what course of action to take. In closing ill reiterate once more that if finasteride isnt stopping your hairloss its most likely due to the drug not reducing adequate type 2 DHT, which dutasteride will in most cases remedy this.

[BaldingHelpMe]

With 0.5mg DUT at a steady state and adequate sulfotransferase activity theres no reason why you wouldnt gain nearly all of your hair back

What is sulfotransferase? And how do I ensure there is enough sulfotransferase activity? I'm also taking dut 0.5mg daily, plus Omega-3 fish oil, vitamin B complex, and vitamin C.

[dm90]

What is sulfotransferase? And how do I ensure there is enough sulfotransferase activity? I'm also taking dut 0.5mg daily, plus Omega-3 fish oil, vitamin B complex, and vitamin C.

It's the enzyme that converts minoxidl into it's active form, minoxidil sulfate. A lot of people lack adequate amounts of the enzyme which is why for some minoxidil grows a lot of hair back while for others it does nothing. There are a few studies that demonstrate hydrocortisone increasing phenol sulfotransferase activity by 3-5 times.

[BaldingHelpMe]

It's the enzyme that converts minoxidl into it's active form, minoxidil sulfate. A lot of people lack adequate amounts of the enzyme which is why for some minoxidil grows a lot of hair back while for others it does nothing. There are a few studies that demonstrate hydrocortisone increasing phenol sulfotransferase activity by 3-5 times.

Is this an enzyme that our body naturally have or is it from Minoxidil? I don't like putting topical stuff on my hair, so minoxidil is not an option for me.

How do I ensure I have enough of these enzymes if I don't use minoxidil?

[dm90]

Is this an enzyme that our body naturally have or is it from Minoxidil? I don't like putting topical stuff on my hair, so minoxidil is not an option for me.

How do I ensure I have enough of these enzymes if I don't use minoxidil?

My apologies I wasn't too clear when I made that statement, the enzyme I mentioned is only relevant, as far as i know, to minoxidil when it comes to hairloss. Minoxidil sulfate is the active form of minoxidil, it is what causes regrowth. If you lack this enzyme minoxidil wont work. However, if you have the enzyme minoxidil can potentially work wonders for your hair. Essentially what I was saying was that If you are one of the lucky responders to minoxidil you can pair it with avodart and potentailly regrowth all of your hair if it was only recently lost. There are very few accounts of this happening but it does show that minoxidil can have a powerful effect. Im sorry for the confusion, many feel that minxodil isnt worth the trouble because of the uncertainty. Perhaps one day applied biology, the company developing the minoxidl response test, will release a product, until then all you can do is try the medication out.

[BaldingHelpMe]

If you lack this enzyme minoxidil wont work. However, if you have the enzyme

So this is an enzyme our body naturally have? I can't apply minoxidl everyday, so I'm not starting it. So without minoxidl, how do i make sure I have enough of these enzyme?

[Sanchez123]

Yeah bro, fin in my eyes is a far worse drug.. Don't ask me why, but I just feel better on dutasteride. No regrowth really.. Actually, the back of my scalp started getting thin and that filled in it seems in just four months. Caught that one early though lol. My temples are slowly receding, but the short minaturized hairs actually are growing out longer on dutasteride.

Dutasteride powder is basically just dutasteride in powder form lol. I bought 10 grams of it so I'll literally never run out. I still take avodart, but like I said if I need to up my dose, it won't break my wallet.

Before I got on dut though I took a 2 month break from AA's so idk if that somehow let me reset in a way from the bad effects of fin? Anyway, dut may be helping and it takes a lot for me to say that. Going to Wait til 6 month mark to Reevaluate if I'm doing better.

Are you on a legit generic? Give it like two weeks of ED usage and you should feel if your responding at all. You really won't see results til 6-12 months just like fin. I started getting less of an itch this month actually so it def takes time.

How is your situation now ziggy?

[blohan]

How is your situation now ziggy?

Has that user had any erection problems?

[cardib]

your libido will go to shit with dut. kiss staying hard goodbye

[Sanchez123]

Anybody got an update?

[noobo]

Could someone please message me who knows how I could get in on a dut groupbuy?