All members who shared PROSCAR into pieces have to consider they messed up with 5AR type I

General Discussion
#1

These are the reasons, why those of you who shared PROSCAR should also keep your mind on:

  1. Active substance is not spread propotionaly within PROSCAR tablet. If you share it into pieces you never know how much PROSCAR is in the 1/4 or 1/5 of it. It is possible that most of finasteride is cumulated even in one quater.

2.Conclusions: When you shared PROSCAR into pieces there is a propability (even if low) that you gave more less 5 mg of active finasteride. This leads to the conclusion that you might have been under the influance of full PROSCAR, which in 5mg dosage also inhibits 5 alpha reductase type I.

  1. Merck also confirmed this propabiltiy even if it previosly was considered as a marketing issue by the hairloss community.

  2. Many of you Guys have similar problems to mine. The difference is that I used DUtasteride 0,5 mg. Finasteride in the dosage of 5 mg is comparible to Dutasteride 0,5 mg.

  3. Assumtions: I think we should really try to investicate what is going on with our 5 alpha reductase type I, which is supposed to be in the brain. Brain gives impulses to all our functions, but 5 alpha reductase type I is responsible for sexual functions. I sense that my problems begin from the brain (I do not know if you focus on this issue enough - those with very long lasting sides).

  4. DHT or Adiol-G would propably not give the clear understending why DHT seems to give low (even if within range) results. These tests does not show clearly which enzyme separated to type I and II produce DHT.

7.Some science: We should investicate if it is possible to have a irreversible cellular damage and how could it even happen if cells are secreted under DNA directions. How would it even be possible for the cell to be partialy irreversibly damaged. If you know any scientists who are involved in biomolecular, molecular projects, it would be great to get some theoritical feedback on this issue.

  1. We should seek for the lab that is doing complexed genetic tests. As far as I know it is extremely expansive.
#2

Please provide proof of this claim.

Where do they confirm this? Please show me, provide a link.

Please provide proof of this claim.

I was under the impression most researchers do not yet understand the function of 5ARI in the brain.

#3

All of my claims were discussed with Merck Sharp & Dohme Propecia representative about 3 years ago.

He told me that it is strongly not recommended to use PROSCAR and share it into pieces because the active finasteride might be not spread within the tablet. That’s why you expose yourself to higher doses. That time I thought (as many others) that this is just a marketing issue, but the more threads I read over www.propeciahelp.com the more I believe it might be the big issue.

I was also trying to compare Propecia to Dutasteride with this representative and he told me that it might have a bigger side effects potential because it inhibits 5AR type I, which is believed to be responsible for sexual functions. This is exactly what he said as a Merck official representative.

I do not know how much DHT type I is inhibited by 5 mg of Finasteride. I read somewhere that it has such potential with a higher dossage. When I will find some information about this thread I will paste it. Maybe I will even call to Merck representative again and ask for that.

If I am wrong about that I will return here and write what are the facts.

#4

So I talked to the Merck representative about Propecia action.

Proscar is similar to Dutasteride 0,5 mg in ability to inhibit 5AR type II, but as you Mew pointed out it does not inhibit type I. Nevertheless he claimed that even Finasteride could have some abilities to inhibit 5AR type I with a much higher doses, never manufactured as a product (just lab tests)

I also spoke to Merck representative and he confirmed that messing with Proscar and sharing tablets is associated with a higher degree of the risk of side effects. The reasons I presented in my first post.
Merck will not be responsible if anyone take Proscar for hairloss.

Anyway I have to clear things up and say that Proscar even if shared has an ability to inhibit 5AR type II to the degree of Dutasteride 0,5 mg, which is more less 90%. It does nothing to type I.

If I could do any logical claims i would say that most guys here and me myself have a problem with the right expression of 5AR type II. I rather think that it is down regulation caused by inflammed liver/prostate. At least I hope it is not worse then that…

#5

majkellos, do you even know what you are talking about? You go from saying there is something wrong with 5AR to adrenal fatigue to Propecia not being able to alter 5AR and back to liver and prostate inflammation changing 5AR. You are debating yourself in a circle and it’s pretty annoying!

If you are having problems with your liver, prostate, hormones, or adrenals GO GET THEM CHECKED. Then come back and let us know. And don’t keep debating your own posts - it makes you sound either crazy or like a troll.

By the way, I thought you were leaving this forum for a year cause you cured yourself with antibiotics?

#6

If you would read carefully my previous posts you would easly realize why I came back here to write “to myself”.

#7

i dunno but maybe this guy is onto something after all because while I was on propecia for only roughly three weeks it seems i recovered slightly and then progressively over the past 10 months all of my problems have gotten worse and worse. Even my sex drive seems to have started to get worse and I’m not even on the drug. Majekos could this have to do witht the fact that my 5AR gene is now shut off and I have used up all the DHT etc that was left in my brain.

#8

I don’t know. NEvertheless I see that it completely doesn’t matter whether you took finasteride or dutasteride before and now have problems. Perheps Glaxo is even more costumer friendly informing people that there are DHT disfunctions associated with a drug.

I used Propecia for almost 5 years. Then I switched to Dutasteride and after 4 months I feelt realy bed. But the most interesting point is that I preety much recovered after most sides… but then about half a year from the point I was clearly off the drug, I woke up one day and I had a total crash… as if the drug did a delayed damage to my system. I found some other people here whose stories are pretty much the same, and this “delayed drop down” occured.

I did liver tests and it might be the liver thing, it would also be pretty much logical then.

Ithappens. I do not realy know. I can only tell you that I read some reports from the people who were going through some liver toxicity/damage. Many people report very strange impact on brain/behaviour associated with their liver desease. Our brain problems could be similar.

Remember that liver is one of the most important organs playing essential role in hormonal/enzymatic conversion. Also remember that fin/dut is metabolised through the liver. If there would be some metabolic blockage/damage in the liver it would obviously impact your brain pushing less DHT into it… and in consequence reducing hairloss, causing brain fog, reducing mental contact with your penis…etc.

This metabolic blockage might be not present in kidneys, testicales, becuse fin/dut has a direct impact on your liver only. In conclusion there is some propability that our dht feedback comes only from testicales, kidneys with a total loss, middle loss from the liver. Possible effects would be all that we actually point out on this forum… (being more less 1/3 of yourself).

I personaly have examined liver and tests are semi bed (ALT,ASP). Now I have to go through some other tests (USG, hepatiitis…). If you read about propable causes of a liver damage, you can easly find that it happens pretty commonly as a negative feedback from the syntetic estrogens intake. Fin/Dut are basicly synthetic estrogens. They mimic some substances found in nature but with a much greater output and bioactivity.

(I read somewhere that finasteride was derived from tuber: the mechanism of action is similar to tuber, do not know if dut is based on any other mechanism of action found in nature, but it is rather possible).

Last word. First thing to diagnose liver problems is when you are allergic to many diatery product. Just to let you start investicate yourself in this field.

Cheers. It is pretty hard to avoid coming back here… S**it.

#9

You state

Problem with this statement is you do not state HOW MUCH it inhibits 5AR1…

The below should help clarify:

google.com/patents?id=x_MXAA … ng#PPA7,M1

PAGE 3:

Although finasteride is not a significant inhibitor of 5
human skin (type 1) isozyme at doses employed in the
treatment of BPH, finasteride does slowly form a comparable
high affinity complex with this isozyme. As determined
by Tian, et al., Biochemistry 33: 2291-2296 (1994), the
second-order rate constant for formation of this complex is 10
4.0xl03 IVT1 s’1’ which is about 1% of the rate constant
against the prostate isozyme. Based on the apparent irreversible
inhibition and on structure-activity considerations,
Tian et al., proposed that finasteride binds to the enzyme
covalently as a Michael acceptor.

www3.interscience.wiley.com/cgi- … 5/ABSTRACT

"Subsequent application of the theory to evaluate the in vivo efficacy data of finasteride indicates low effective concentration of finasteride at the inhibition sites and suggests complete inhibition of 5AR 2, but insufficient suppression of 5AR 1 at the clinical doses."

So it seems that yes, Finasteride does inhibit 5AR-1, but at the dosages we were taking it was likely VERY, very minimal… so much to probably not even be concerned about. The drug is primarily a 5AR-II inhibitor, and is marketed as such. Dutasteride on the other hand inhibits both very strongly.

See my last post here about this for some clarification:

propeciahelp.com/forum/viewtopic.php?t=761

#10

Yes, but do not get so focused on the difference between fin and dut. We are in the same situation after long term regimen with synthetic estrogen-like drugs.

I am rather getting more and more concerned that my situation is due to the long term suppression of my auto immune system due to DHT suppression. Good example is the presence of chlamydia pneumoniae which is present in my body (IGG–>4 times + range). Pneumoniae affects central nerve system and is present in many tissues. This may be the reason for intracellular changes that I may be going through.

After getting an official report from Glaxo world wide emergency room (read in a new topic in a medical section) I am getting more and more concerned about pneumoniae and some different bacteria that might be also present and making some other intracellular tumors. I am also doing a stool peptites tests by the next week.

5AR is a molecule present within cells. This might also explain why I get those digestive disorders, permanent gas, skin lipids problems and many many more…