Cautious & safe way to start Propecia/Finasteride...........

zzzzz

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There is no point in taking a lower dose than 1mg to reduce sides. Inhibition is the same regardless of dose at any reasonable amount.

There is no point in taking propecia over generics
 

Donny J

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There is no point in taking a lower dose than 1mg to reduce sides. Inhibition is the same regardless of dose at any reasonable amount.

There is no point in taking propecia over generics
you've been saying that a lot on these boards lately, but I'm yet to see any proof to your claim. We all know that .25mg inhibits 85% of DHT as opposed to 1mg. Knowing that this has been proven, how can you say that using .25mg won't give your fewer sides than if using 1mg?
 

xRedStaRx

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There is no point in taking a lower dose than 1mg to reduce sides. Inhibition is the same regardless of dose at any reasonable amount.

Not necessarily. There was less reported side effects on lower doses, in both frequency and quantity.
 

Ventures

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Not necessarily. There was less reported side effects on lower doses, in both frequency and quantity.


Do you know maybe why finasterid inhibition curve has zero-flat response ? http://www.propecianow.net/wp-content/uploads/2013/08/propecia-dht-inhibition-curve.jpg

Why do doses of 0.2 mg and more have almost the same effect ? I mean, if you use 5mg finasteride (1 Proscar pill) then you would, according to my logic, inhibit more 5-ard enzymes which would result in more DHT suppression then with 0.25 mg because 5mg of finasteride contains more active substances which then bind to 5-ard and disrupt the conversion process.
 

xRedStaRx

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Do you know maybe why finasterid inhibition curve has zero-flat response ? http://www.propecianow.net/wp-content/uploads/2013/08/propecia-dht-inhibition-curve.jpg

Why do doses of 0.2 mg and more have almost the same effect ? I mean, if you use 5mg finasteride (1 Proscar pill) then you would, according to my logic, inhibit more 5-ard enzymes which would result in more DHT suppression then with 0.25 mg because 5mg of finasteride contains more active substances which then bind to 5-ard and disrupt the conversion process.

Because the amounts of 5-AR II in an average male get almost completely bound by finasteride molecules starting at single doses of around 2.5-5 mg, or every day dosing of 0.2-1 mg of finasteride.
 

Ventures

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Because the amounts of 5-AR II in an average male get almost completely bound by finasteride molecules starting at single doses of around 2.5-5 mg, or every day dosing of 0.2-1 mg of finasteride.


But I do not understand this part: Accroding to MERCK clinical trials 1 mg finasteride inhibits mean (serum) DHT level by roughly 70%. So, there is 30 % left. And why doesn't next 1 mg or even 0.5 mg finasteride (in single dose) inhibit the rest available DHT ?

You mentioned doses of 0.2 mg of finasteride and more allows all 5-AR II to get completely bounded. Only logical clue would be that rest available DHT after administration of 1 mg finasteride would be from 5-AR I, right ? finasteride doesn't inhibit 5-AR I, so it is DHT Type 1 which is available after 1 mg finasteride ?
 

xRedStaRx

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But I do not understand this part: Accroding to MERCK clinical trials 1 mg finasteride inhibits mean (serum) DHT level by roughly 70%. So, there is 30 % left. And why doesn't next 1 mg or even 0.5 mg finasteride (in single dose) inhibit the rest available DHT ?

You mentioned doses of 0.2 mg of finasteride and more allows all 5-AR II to get completely bounded. Only logical clue would be that rest available DHT after administration of 1 mg finasteride would be from 5-AR I, right ? finasteride doesn't inhibit 5-AR I, so it is DHT Type 1 which is available after 1 mg finasteride ?

Right.
 

zzzzz

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Not necessarily. There was less reported side effects on lower doses, in both frequency and quantity.

what is the difference in sides between doses?

for ex:

.25mg vs 1mg
5mg vs 1mg
.25mg vs 5 mg
 

xRedStaRx

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what is the difference in sides between doses?

for ex:

.25mg vs 1mg
5mg vs 1mg
.25mg vs 5 mg

I wouldn't go above 1 mg either way because it's effect on hair is insignificant.

The difference between 0.2 and 1 mg is probably the severity of side effects, or none vs minor ones.

Interminent doses (EOD, E3D) has also been known to reduce potential side effects, while keeping hair results roughly the same.

The former is purely anecdotal. The latter is based on different studies that I've went through by memory.
 

Ventures

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And I didn't understand why serum DHT level doesn't represent true inhibition value? You mentioned on another thread that serum DHT level consists mostly of DHT excreted from tissues as some kind of excess/waste form. This fits with known fact that DHT is mostly generated locally in tissue, and has mainly the effect only in tissues where it has been produced.

Can you give more concise explanation what you think when you say that ?
 

xRedStaRx

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And I didn't understand why serum DHT level doesn't represent true inhibition value? You mentioned on another thread that serum DHT level consists mostly of DHT excreted from tissues as some kind of excess/waste form. This fits with known fact that DHT is mostly generated locally in tissue, and has mainly the effect only in tissues where it has been produced.

Can you give more concise explanation what you think when you say that ?

DHT is locally produced in tissue where the organs needs it, this is why DHT is an autocrine, not an endocrine hormone. So any DHT in the blood is a result of 5-AR conversion of T to DHT, and "leakage" of the DHT molecules systemically, where it has a short half life of only a couple of hours. The reason why serum DHT levels go up is either because of increased 5-AR activity, or saturation of ARs near the target tissue. The prostate is thought to contribute to most of serum DHT levels because it is an androgen intensive organ. You could have basically full saturation of DHT concentrations inside hair, scalp, skin, prostate tissue, but little to no DHT in the blood. This is why serum DHT levels is only a proxy for 5-AR activity, and not a reliable measure.

In fact, men with higher serum levels of DHT were statistically less prone to balding than otherwise.
 

Ventures

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DHT is locally produced in tissue where the organs needs it, this is why DHT is an autocrine, not an endocrine hormone. So any DHT in the blood is a result of 5-AR conversion of T to DHT, and "leakage" of the DHT molecules systemically, where it has a short half life of only a couple of hours. The reason why serum DHT levels go up is either because of increased 5-AR activity, or saturation of ARs near the target tissue. The prostate is thought to contribute to most of serum DHT levels because it is an androgen intensive organ. You could have basically full saturation of DHT concentrations inside hair, scalp, skin, prostate tissue, but little to no DHT in the blood. This is why serum DHT levels is only a proxy for 5-AR activity, and not a reliable measure.

In fact, men with higher serum levels of DHT were statistically less prone to balding than otherwise.

Yes, everything what you said makes sense. But if DHT produced locally in scalp (or to be more precise inside follicles ) is the one which is the most dangerous to hair, why topical finasteride or dutasteride show not to be so effective? Is it because finasteride and dutasteride must be metabolised by certain enzymes in a liver in order to be effective and/or there is not great absorption in scalp area which means finasteride when applied locally on scalp is not able to reach dermal papilla ? What is your opinion ?
 

xRedStaRx

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Yes, everything what you said makes sense. But if DHT produced locally in scalp (or to be more precise inside follicles ) is the one which is the most dangerous to hair, why topical finasteride or dutasteride show not to be so effective? Is it because finasteride and dutasteride must be metabolised by certain enzymes in a liver in order to be effective and/or there is not great absorption in scalp area which means finasteride when applied locally on scalp is not able to reach dermal papilla ? What is your opinion ?

Using topical finasteride is pretty meaningless, any systemic absorption would still be the same as swallowing it, since it is extremely effective, even at micro doses.

The reason why is doesn't work well has nothing to do with the liver, finasteride can work just as well through IV injections. The problem is we are not using a proper vehicle to properly penetrate the deep layers of the skin and reach the root DP.

In order to develop a novel transdermal drug delivery system that facilitates the skin permeation of finasteride encapsulated in novel lipid-based vesicular carriers (ethosomes)finasteride ethosomes were constructed and the morphological characteristics were studied by transmission electron microscopy. The particle size, zeta potential and the entrapment capacity of ethosome were also determined. In contrast to liposomes ethosomes were of more condensed vesicular structure and they were found to be oppositely charged. Ethosomes were found to be more efficient delivery carriers with high encapsulation capacities. In vitro percutaneous permeation experiments demonstrated that the permeation of finasteride through human cadaver skin was significantly increased when ethosomes were used. The finasteride transdermal fluxes from ethosomes containing formulation (1.34
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±
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0.11 μg/cm2/h) were 7.4, 3.2 and 2.6 times higher than that of finasteride from aqueous solution, conventional liposomes and hydroethanolic solution respectively (P
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<
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0.01).Furthermore, ethosomes produced a significant (P
x2009.gif
<
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0.01) finasteride accumulation in the skin, especially in deeper layers, for instance in dermis it reached to 18.2
x2009.gif
±
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1.8 μg/cm2. In contrast, the accumulation of finasteride in the dermis was only 2.8
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±
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1.3 μg/cm2 with liposome formulation. The study demonstrated that ethosomes are promising vesicular carriers for enhancing percutaneous absorption of finasteride.
 

Blackber

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If this is true why don't most people just take .25mg?

I'm not trying to be abrasive just honestly asking a question.

- - - Updated - - -

I think we're getting off topic on this thread.

There are plenty of other threads that debate this.

I'm looking for feedback on my OP (like whether tapering yourself into the drug is a smart idea) and new suggestions.
 

xRedStaRx

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If this is true why don't most people just take .25mg?

I'm not trying to be abrasive just honestly asking a question.

I can think of a few reasons, but mainly because it doesn't generally make a difference, besides the hassle of cutting down doses that small from a 5 mg pill. Most just opt for (0.5, 0.625) or larger doses. Either daily or EOD.
 

Blackber

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I just started finasteride 1mg two days ago and have/will be cutting the pills down to .25mgs per day for the first few weeks/months.

Do you think that is a cautious/safe idea?

I do plan on ramping up to .50mgs or 1mg per day but slowly.

You mentioned that "it doesn't make a difference".... Are you saying the efficacy is the same, lower dose vs. higher dose? Or do you mean .25mg of finasteride is not enough to make a difference in hair loss?

Are there any people that have good results on lower dosages of finasteride? (.50mg per day for arguments sake)

Thanks in advance!
 

xRedStaRx

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I just started finasteride 1mg two days ago and have/will be cutting the pills down to .25mgs per day for the first few weeks/months.

Do you think that is a cautious/safe idea?

I do plan on ramping up to .50mgs or 1mg per day but slowly.

You mentioned that "it doesn't make a difference".... Are you saying the efficacy is the same, lower dose vs. higher dose? Or do you mean .25mg of finasteride is not enough to make a difference in hair loss?

Are there any people that have good results on lower dosages of finasteride? (.50mg per day for arguments sake)

Thanks in advance!

I've thickened the temples a little using 0.5-0.625 mg EOD personally. So yes, anything more than and including 0.2 mg ED should be enough.

There is no 'safe' dose to take. I guess you could take bigger doses intermittently instead if you're worried, like I do.




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