Plenty of guys get worse if they dont also
Yeah, I know, I wasn’t saying this was exclusively responsible just noting a trend.
I know dude, i think liquor could have played a part in some cases but for me…it was over either way
I have stumbled across two articles which may interest some. The first one is about a woman who fell pregnant 90 days after the cessation of her Accutane course (arguably should have been out of her system in 1 month): only to find that the foetus had been effected by the drugs teratogenic effects.
ncbi.nlm.nih.gov/pubmed/19961047
This second article discusses the potential of licensed drugs and natural supplements to cause hepatotoxicty. This is the full version:
These are prime examples of how things get stored in your liver and tissues, long after they have left your blood stream.
-Letsconviniance uses oxbile for 5 months…gets better.
-Pink floyd starts juicing including beets…“something changes after 3.5 years” Beets stimulate/increase bile flow.
-Goingtowin points out a few recoveries that use tribulus terrestris…tribulus increases the flow of bile.
Considering this study why wouldnt fin be stored in our livers along with excess estrogen(a steroid hormone), copper, i have had consistantly high copper blood post fin, to my knowledge i am the only one tested. Also why are some members getting worse over time and why do some have brief recoveries…“My body decided not to be androgen insensitive for a couple of days” wtf?
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This is an old article that discusses many of the hormonal inbalances many here have and ties them to altered liver function:
Here is another article citing what Tim mentioned above; it clearly mentions that impaired drug metabolism due to inhibition of CYP3A4 can cause long lasting effects and even fatal toxicity. It seem quite evident that the theory of faultering metabolism and subsequent drug induced liver damage (precipitated by finasteride and accutane inhibiting there own metabolism) go quite far in explaining a lot of what has happened; it also explains the no alcohol policy that most here abide to. The punch line goes thus: “Many of these drugs are also mechanism-based inhibitors of CYP3A4, which involves formation of reactive metabolites, binding to CYP3A4 and irreversible enzyme inactivation.”
Did you put this in the studies section? I agree it explains a lot for a significant number of us who took the drug and had progressive sides develop over a long period of time.
Martin, I assuming most people here have read it given the controversial name of the thread; but, I will put it where you suggested later today. What I find disconcerting, is how little credence people give to the fact that the liver is essentially the hormonal control centre of the body. I know we all refer to Finasteride and Accutane as poison; but, in the overwhelming number of cases (of course there are always exceptions) it is our bodies which converted it to poison: given the rare group of people we are.
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hi.
Where does it say accutane can inhibit its own metabolism? thanks
Accutane is implicated in inhibiting it’s own metabolism here:
I would like to thank Former for this article which explains that DHT is primarily converted to 3 Adiol G via the liver
I can see a potential mechanism where finasteride inhibits its own metabolism and is stored in the liver.
We come off the drug, peripheral 5a2 is restored, recovery is had, but due to the finasteride in the liver 5beta reductase is continued to be effected, which would down regulate the Pregnane X receptor (PXR) ongoing.
Thus slowing our metabolism of everything ongoing.
Via the studies i have posted the PXR indirectly influences sex hormone receptors when their is an endocrine disruption.
I also wonder about this study.
[Size=4]Identification of human cytochrome P450 isozymes responsible for the in vitro oxidative metabolism of finasteride.[/size]
ncbi.nlm.nih.gov/pubmed/8654202
Came out in 1995, just about the time merck were trying to get Propecia on the market, and well, well, well look who run the study, Department of Drug Metabolism, Merck Research Laboratories, Rahway 07065, USA. 
You might find this of interest then, particularly the last sentence:
INHIBITION OF HUMAN STEROID 5B-REDUCTASE (AKR1D1) BY FINASTERIDE AND STRUCTURE OF THE ENZYME-INHIBITOR COMPLEX
viewtopic.php?f=8&t=2703
Yeah i know mew, its diabolical. I hope you fellas are feeding all this to your lawyers, along with the partial inhibition of Palmitoylethanolamide.
Also mew they say “at high dose” but isnt it (finasteride) a flat dose from about 1mg upwards?
ok
so what might be the treatment?
Yes it imply’s that the liver is responsible for 80+% of circulating adiolg.
Tim, it is likely to go the other way as well. We know that Pregnane X receptor activity is what protects the body from lipophilic xenobiotic accumulation. In theory, dysregulation (down regulation) of PXR would induce a loss of sufficient detoxification, and subsequently storage of the drug. This, of course, would lead to greater toxicity. Funnily enough PXR is referred to as a promiscuous receptor, due to the broad spectrum of lipophilic xenobiotics which activate it. I read that as potentiating dysregulation.
I also want to say that this putative storage component of this theory should not be viewed as the end, but, rather the beginning of the problem. In a word: Storage is not the root of the problem now (years later for some), but a precipitator, and a co-conspirator in compromised drug metabolism at the outset.
toxicology.usu.edu/endnote/2444S.pdf
merckmanuals.com/home/drugs/administration_and_kinetics_of_drugs/drug_distribution.html
Drug storage due to Phospholipidosis:
Also need to consider mitochondrial drug storage which may interfere with the determination of pharmacokinetic parameters (distribution volume, plasma concentration, and half-life):
notworthit, propecia is not being ‘stored in liver cells’. It was an air-head idea 2 years ago and still is now.
Taking quotes out of context from papers you dont understand wont change that.
A possible problem with the end metabolism of the drug is something different.