So there’s been a lot of talk about antibiotics being a culprit as onsetting PFS across the forums. I’ve been looking for the past 8 or so hours into the enzyme CYP3A4. CYP3A4 is the enzyme responsible for metabolizing and getting rid of finasteride from our bodies. I’ve just discovered that many antibiotics downregulate the CYP3A4.
Also, anti fungals downregulate it as well (very potently I might add, on FDA’s website it’s talked about how the active ingredient in Nizoral is a potent inhibitor of this enzyme).
Also interesting to note there are some anti bacterials that increase CYP3A4. Also, IHP had a recovery using Nyastin, where does this play here? Does it upregulate or downregulate CYP3A4, I’d imagine it would do one or the other.
Is it possible we were taking finasteride everyday, and the CYP3A4 was upregulated in order to get this drug out of our system. But, when some people took either anti biotics or anti fungals or something else, the CYP3A4 got downregulated, thus making it ineffective to finasteride in our body. After the drug ran loose in our bodies, perhaps it has left the liver detoxification phases all out of wack and left us in a state of PFS. Maybe the liver detox’s never got fixed and we still have finasteride in our body?
Now I’m not sure honestly if downregulating is a good thing once you have PFS or upregulating is a good thing when you have PFS. You can see milk thistle is on this chart, but unfortunately it is not known how it effects this. We all know that milk thistle effects us positively at first, but then negatively.
Here’s another interesting tidbit: St John’s Wart speeds up CYP3A4, but CYP3A4 is also in charge of metabolizing testosterone. A user on our forum used St John’s Wart and talked about how his condition was improving greatly, but his testosterone was dipping. This could be why people who get back on finstasteride seem to do better. Perhaps it’s is upregulating the CYP3A4 and for whatever reason, it is making people better, maybe the liver detox systems are starting to work on point again from being out of wack from taking finasteride in the first place.
Now the question is: Does upregulating or downregulating CYP3A4 help us or hurt us?
I’m not sure if upregulating it is just further delaying the body’s natural ability to find homeostasis or it is actually helping?
Is finasteride still in our bodies? I don’t know. Maybe. But there is without a doubt something wrong with the liver’s detoxification systems that is for sure. Whether it’s because fin is still inside us, or fin left us in a state of a non working liver, it’s important to get it fixed.
for sure finasteride had some influence on my liver. I have said this before and I wondered if it was connected, because at the moment I quit (around 2 weeks later) I did blood exams and GAMA-GLUTAMIL TRANSFERASE was at 9U/L while the range was 8-61.
I would like to know if someone else made this exam upon quitting? I think I asked this before even…
guys, we all suffer from the same problem here. if any of you could look into and get the Functional Liver Detoxification Profile test, we would have a much better picture of what is wrong with our livers along with some potential options to go about fixing it. if not, we could just be running in a big negative feedback loop.
When I was looking into this a few months ago the only thing that was proposed at aiding Phase II clearence was Calcium D-Glucarate. Don’t know how valid that is, but I’d tried a bottle without much improvement.
I guess theoretically we want to inhibit phase 1 and accelerate phase 2. Grapefruit is effective at doing the former, but I actually felt a lot worse after ingesting a load of it. Plenty of people on here have also negative experience with Milk Thistle which has similar mechanisms.
The binding hormones are predominatly synthesised in the liver, so it’s plausible that poorer clearence is inducing an increase in excessive SHBG, Albumin, Transcortin etc.
These all have negative effects on the free hormonal balance between androgens and estrogen, since testosterone has a lot higher affinity toward them.
guys, ı read somethıng. Low allopregnanolone decrease cyp3a4 actıvıty.
thıs pılls decrease allopregnanolone we know that and thhıs cause decreased cyp3a4 actıvıty. When cyp3a4 actıvıty get low gut doesnt absorbe drug normally. And thıs cause of a kınd of drug posıonıng. Does thıs sound stupıd?
I was on a heavy dose of amoxicillin for approx one year before my pfs started. I took the amoxicillin for severe acne that I had at the time. Dermatologist had me on antibiotics as a long term acne treatment because the only other alternative was to put me on accutane which he did no like putting young guys on. Go figure if only every doctor was that smart to avoid giving out DHT inhibiters we would not be in this mess.
Also was on the amoxicillin during the time the pfs started as well.
My PFS start after several Clarithromycin cycles for Hpilory. Clarithromycin is a strong inhibitor of CYP3A4 enzimes. for me, was the trigger of my PFS
this enzyme is responsible for metabolizing estrogen and testosterone.
is possible that our body is not metabolizing properly some hormones.
it is possible that other substances can interact with the enzyme that has not been documented. Alcohol? a common drug.
