The Antibiotic Connection - CYP3A4

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.

I had a similar experience with grape fruit seed extract.

Are you basing the phase 1/phase 2 results from the saw palmetto guy? Do you know if any PFS people have done this test? I’m trying to locate this.

you know one guy claım that he ıss recovering wıth rifampicin.

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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?

not stupid at all. low allopregnanolone is one of the problems for sure…

our allepregnanolone levels decreased permanantely, thıs decrease pxr actıvasıon and decrease cyp3a4 actıvıty. Lets see cyp3a4 fonctıons

• monooxygenase activity • monooxygenase activity • steroid binding • iron ion binding • steroid hydroxylase activity • electron carrier activity • oxidoreductase activity • oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen,
reduced flavin or flavoprotein as one donor, and
incorporation of one atom of oxygen • oxygen binding • enzyme binding • heme binding • vitamin D3 25-hydroxylase activity • taurochenodeoxycholate 6alpha-hydroxylase activity • caffeine oxidase activity • metal ion binding • albendazole monooxygenase activity • quinine 3-monooxygenase activity • testosterone 6-beta-hydroxylase activity • vitamin D 24-hydroxylase activity

also scıentısts fınd evıdence cyp3a4 of central nervous system

I never took antibiotics while on fin, it is not the culprit

i took Clarithromycin while on fin

did you took any of this drugs while on fin

(Inhibitors)

en.wikipedia.org/wiki/CYP3A4

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.

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makes a lot sense this theory.

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.

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there is a guy that took Rifampicin and recovery.

Rifampicin increase estrogen metabolism.

I did I was on doxycycline right before I took 0.2mg of finasteride

It’s not only about antibiotics. Many people (including me) have used finasteride with ketoconazole (strong CYP3A4 inhibitor).

What would that do

Its almost certain that the CYP3A4 enzyme has become low in our liver. I wonder why no body is looking into it. Why no further works has been done?

Bump. It does seem like CYP3A4 has something to do with PFS. Like we all had diminished CYP3A4 activity due to genetics or antibiotics (which i had taken several times in my life for acne) or antifungals or whatever. And then upon administering the finasteride, our bodies tried ti eliminate it from our system with the help if that enzyme which had been previously been weakened, causing the fin to run amok, making us feel great in the process until some other mechanism came in to shut the whole thing down.

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Glad you bumped this because there definitely might be something to this one and thanks to the user up there who showed what it is involved with.

I actually now am morbidly curious as to how I’d react to a dose of testosterone even though based on my experiences already I am 99 percent sure that would be a horrible idea and crash me permanently. Every time I take anything remotely steroidal I get both benefits and near misses with crashes and sexual functioning specific problems. Recently I wanted to see what would happen if I ate a massive amount of asparagus all at once because of that compound protodioscin. Took 2 whole bags, lightly cooked them, and chowed down. Huge increase in energy, I mean I felt like the hulk and my social ability and desire shot through the roof, I also had no more anxiety. It completely obliterated it temporarily. There was one problem though, dick would not work. It just wouldn’t respond to anything in thay state. The next day I was much stronger and some of the benefits in anxiety reduction and increased social functioning lingered. Though the next day the ED was still an issue and it didn’t get better till I was out of that state again and back to my previous baseline with not so great but functioning responsiveness sexually but with no more benefits I got from the large amount of asparagus.

Interesting that vitamin D3 is also handled by it because the same pattern erupts but only vitamin D3 has much more unstable effects and I simply can’t do it anymore. I recently tried it topically as I wanted to see what happened and it was a disaster. I took 1000 iu of my MCT oil based vegan D3 drops and rubbed them into my wrist. I didn’t get any genital shrinkage like I did from oral dosages but I did initially get as expected a spike in ED though it wasn’t too bad. I noticed though that I had much more sensation down there and when I did get it going, I had one of the most pleasurable orgasms I had in a while. I got some weird dry mouth on and off throughout the day that decreased in intensity as the days passed since the dose. The dose initiated extremely anxiety all day long, my social functioning was replaced with sheer exisstencial terror and I felt like I had drank 50 cups of the worst coffee of all time while all the same I somehow felt more mentally dull and a bit anhedonic. Wasn’t really getting anything out of anything I previously enjoyed in this state. That night I had insomnia, I was barely able to even just lay down and relax. When I did I had horrible migraine like dreams and woke up feeling like I didn’t get any rest at all. This went on for 2 days with decreasing intensity till today where I’m feeling relatively ok if still a bit anxiety ridden and string out feeling, functioning socially was a bit rough today but nothing like the past couple. Sexual functioning and sensitivity is normal again for what it’s been maybe slightly more reactive actually on the bounce back. Had a little dry mouth this morning but nothing crazy. Very strange, I wonder what is going on here.

I think this could be plausible…therefore taking a CYPA34 inducer like St John’s Wort can help the enzyme get back to functioning again

In short we need to find a lab which can measure our CYP3A4 and other P450 enzymes.

io penso che il CYP3A4 possa essere più alto nei casi in cui si verifica basso T e perdita muscolare con dolori articolari e debolezza in sostanza è come se il nostro organismo cercasse di liberarsi dalla finasteride che evidentemente ancora circola nel nostro corpo oppure potrebbe essere una azione del 5beta reduttasi anch’esso inibito dalla finasteride che determina l’attività del CYP3A4. Forse dopo la sospensione della FINA riparte il 5beta che promuove l’attività dell’enzima CYP3A4 ma il corpo è molto intossicato e per questo vi è una degradazione di T, Prog, Cortisolo e tanto altro di cui il nostro corpo ha bisogno. Questo potrebbe spiegare le cadute dopo le terapie sostitutive. Per quanto mi riguarda ho trovato benefici con un debole inibitore del CYP3A4 il Pantoprazolo però ho dovuto sospendere perchè causa alla lunga danni ai reni. Non è dato comprendere come si può regolare l’attività del fegato che si attiva in modo eccessivo per depurare il corpo di fatto il fegato non sintetizza gli ormoni ma li degrada causando tutti i sintomi che ognuno lamenta … questo spiegherebbe perchè in generale ci si affida al tempo molto tempo nell’arco del quale il fegato si ripara … nel mio caso sono seriamente preoccupato di aver creato un danno permanente al fegato o di avere comunque una situazione di progressivo peggioramento dato che ho preso FIN sempre in associazione con inibitori del CYP3A4. Qualcuno ha idee in merito???

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