Dutasteride doubles the half-life of Oral T and TE

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Oral Testosterone in Oil Plus Dutasteride in Men: A Pharmacokinetic Study

Coadministration of D with oral T or TE significantly increased the 24-hr average serum T levels compared with administration of T or TE alone [average serum T after 400 mg dose, 8.7 ± 3.0 nmol/l (T) and 8.3 ± 5.7 nmol/l (TE) vs. 16.1 ± 5.8 nmol/l (T +D) and 15.0 ± 8.8 nmol/l (TE + D); P < 0.05 for T vs. T and D].

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(The full text is easy to find, but I'm not allowed to post URLs yet)

Does anyone suspect that dutasteride may have this same effect on other oral steroids, like Var, or is there something special about oral T that makes this possible?

What is the mechanism for increasing the half-life? Is it a result of the T not being able to convert to DHT ?

lol, that should have been obvious.

My bad.

The direct inhibition of test to DHT has little to do with this. DHT conversion overall is fairly low, even with a fully functioning 5a-r enzyme.

But I'd need to look at the study and see exactly what form of test they are using (oral test doesn't tell me much) to make an accurate guess.

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Originally Posted by Bonaparte

The direct inhibition of test to DHT has little to do with this. DHT conversion overall is fairly low, even with a fully functioning 5a-r enzyme.

But I'd need to look at the study and see exactly what form of test they are using (oral test doesn't tell me much) to make an accurate guess.

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That being said, do you have an educated guess?

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Originally Posted by Bonaparte

The direct inhibition of test to DHT has little to do with this. DHT conversion overall is fairly low, even with a fully functioning 5a-r enzyme.

But I'd need to look at the study and see exactly what form of test they are using (oral test doesn't tell me much) to make an accurate guess.

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Have you looked into it?

Don't get me wrong, I'm sure there's a feed-back loop of some sort wherein your brain sees less DHT, and so you make more T.

That said, why wouldn't inhibiting 5ar increase T's half-life?

At that point you'll have to eliminate that T in some other way.

Now that I think about it, anabolics are given and anabolic/androgenic ratio, but isn't much of that denominator determined by the reduction of the gear's original molecule into something else by 5ar (e.g. dbol becomes 5ar-dbol, or something)?

So shouldn't inhibiting 5ar actually not only increase the half life of oral T, but also increase the half-life of any AAS that can reduced by 5ar?

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Originally Posted by xelnaga

That being said, do you have an educated guess?

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Well, it could compete with the enzymes that break down esters, or something of the sort.

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Originally Posted by Furious.George

Have you looked into it?

Don't get me wrong, I'm sure there's a feed-back loop of some sort wherein your brain sees less DHT, and so you make more T.

That said, why wouldn't inhibiting 5ar increase T's half-life?

At that point you'll have to eliminate that T in some other way.

Now that I think about it, anabolics are given and anabolic/androgenic ratio, but isn't much of that denominator determined by the reduction of the gear's original molecule into something else by 5ar (e.g. dbol becomes 5ar-dbol, or something)?

So shouldn't inhibiting 5ar actually not only increase the half life of oral T, but also increase the half-life of any AAS that can reduced by 5ar?

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We're talking about exogenous T here. Your body can't make more of it.

And when you inhibit 5-ar, you increase aromatase activity (which is half of why I hate the stuff).

Dbol is 5-a reduced to M1T, but at a negligible rate. Same goes for EQ's conversion to DHB (1-Test).

I'm having trouble responding cuzza the spam filter.

Why does it matter if were talking about exogenous or endogenous T?

I cited research showing that 5ar inhibitors increase the half-life of oral T, but there's also research showing that 5ar inhibitors increase endogenous T. It seems reasonable that most of that effect could be explained by the elimination of 5ar.

Similarly, do 5ar inhibitors increase aromatization, or is that increase a result of having more T available to be converted? 5ar inhibitors can cause gyno, but not nearly as much as exogenous T or T-like molecules.

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Originally Posted by Furious.George

I'm having trouble responding cuzza the spam filter.

Why does it matter if were talking about exogenous or endogenous T?

Because the study states that Finasteride doubles the half-life of exogenous T. So we're not talking about some feedback mechanism causing an increase in T production.

I cited research showing that 5ar inhibitors increase the half-life of oral T, but there's also research showing that 5ar inhibitors increase endogenous T. It seems reasonable that most of that effect could be explained by the elimination of 5ar.

Not at all. 5a-reductase only accounts for a small portion of testosterone's metabolism. The majority of it binds to ARs as Testosterone and is never converted to estrogen or DHT.

Similarly, do 5ar inhibitors increase aromatization, or is that increase a result of having more T available to be converted?
Both. DHT is needed to antagonize estrogen and its effects in the body. Get rid of it and shit can get out of hand in a hurry.

5ar inhibitors can cause gyno, but not nearly as much as exogenous T or T-like molecules.
We're talking about combining the 2.

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bolds

Still, it seems perfectly reasonable that 5ar inhibitors would also increase the half-life of injected T. You don 't see something special about oral T, or endogenous T, do you?

I was on propecia for 8 years...

Here is what my blood tests looked like on Propecia over many years.

Total T 1000ng
E2 lvl through the roof over 200



1 year off propecia

Total test 500

E2 37.


ENdo basically told me , by blocking conversion of test to DHT this leaves more total T because its not getting converted... Then your body trys to counter act thyis by making more estrogen..


That SH!T completly Fkced me up... Been off Propecia for close to 4 years now i think...