Proof that finasteride is STILL inside us?

Hey guys – I have intentionally boycotted the forum for a long time – I could not deal with the negativity and in-fighting any longer. It’s done me a lot of good to go away indefinitely and work on other parts of my life so that when the cure arrives, I’m ready to go. But I have something that I hope you’ll give some thoughtful consideration – something I thought compelling enough to break my fast from the forum.

I have (borrowed and re-visited) the idea that finasteride is STILL in our systems and here’s why:

Venceremos has been suffering from fluoroquinolone antibiotic-related tendon damage since his prostate treatment of over one and a half years ago. He recently relayed that he had HLPC testing done which confirmed that he still had levaquin circulating in his blood, after only having taken TWO 500mg doses of it. I repeat: ONE AND A HALF YEARS AGO. TWO DOSES. STILL IN HIS BLOOD. Interestingly enough, he took fifteen 1000mg ciproflocaxin pills, yet has a lower concentration of that in his system. He was not able to test for levels of the other antibiotics he took.

If a class of drugs which is known to cause serious, lasting, debilitating side effects like fluoroquinolone antibiotics is confirmed to be in sufferers’ blood stream (many confirmed cases), more than one and a half years after consumption in this particular case – how can we not take seriously the possibility that finasteride, a drug known to inhibit its own metabolism via inhibition of the CYP3A4 liver enzyme (ncbi.nlm.nih.gov/pmc/articles/PMC2740403/) - which ALSO is known to cause serious, lasting, debilitating side effects — is still in our systems?

I’ll summarize that last thought again:
ncbi.nlm.nih.gov/pmc/articles/PMC2740403/
“Importantly, finasteride itself is metabolized by CYP3A4, suggesting that high dose finasteride might prevent its own metabolism”

Separately, we know from Merck’s own studies that there is no difference between high and low dose finasteride.
[Size=4]
The theory of finasteride STILL being present in our systems would explain why:[/size]

-some people are hit after just a few doses, some after several months, some after several years (we all have different constitutions, different metabolisms, different enzymes, different genetic makeups, different detoxification capability, and so forth)

-some people experience fleeting, temporary recoveries via seemingly disparate means: milk thistle, fasting, heavy metal detox, juicing. (toxins/pharmaceuticals simply get recirculated. *See the attached Scientific Study on Toxicology and the excerpt at the end of this post on enterohepatic recirculation)

- some long-term TRT users (golf, enden, one other 2 year Dr. Crisler patient who’s name escapes me) are able to stimulate 5AR/overcome any suppression or toxicity from still-present fin and have working, functional sexual recoveries

[b]-Nystatin (which I have received confirmation up-regulates 5AR) helps so many who try it - and does not create resistance to (gasp! lol) candida with multiple starts/stops. But causes regression once stopped (too soon?)

-IHP – who both detoxed (bentonite clay, chinese herb flushes, zeolite, bentonite clay, IR sauna) AND took copious amounts of Nystatin – would seem to have both purged his system of fin AND up-regulated 5AR

-IHP completely recovered sexually, but not mentally (still some brain fog, although it’s slowly improving he just reported to me). Why? Perhaps because he had started with fin, but then moved on to dutasteride which inhibits 5AR1 as well (among other areas, more present in the brain), and “only” up-regulated 5AR2 via Nystatin? Or didn’t clear enough from his system?

-those that did heavy metal cleanses temporarily felt better (elimination organs backed up w/ metals were cleared allowing toxins like fin to shuttle around)

-some of the anecdotal (but hard to verify) recoveries using GHB/Xyrem coupled with Nystatin occurred

-PFS patients suffer so many comorbid conditions including immune dysfunction, infections, adrenal issues, thyroid issues, etc. — chronic 5AR suppression would have a cascade effect on the immune system, skin, digestion and beyond

-personally, I felt my best, almost like I was turning a corner (was able to get half-aroused again and “only” need one 20mg cialis dose to have sex) while combining the following therapies: routine H202 IV treatments (along with glutathione – liver pathway detoxifier), nystatin, juicing, colonics. When I stopped/slowed these things (and when I tested masturbation more), things regressed until I hit rock bottom again.[/b]

Again, this would explain one of the biggest puzzles – how can ANY substance act so quickly/permanently in some, and take so long to take others down – and exact such persistent side effects? And how can so many disparate means of treatment (from TRT to Nystatin to Juicing to Milk Thistle) be connected?

[Size=4]In my view, there is enough here to warrant/demand that the PFS Foundation devote serious attention to ruling out this possibility. Currently, there is just one institution that has mapped the finasteride molecule – but if an organized bunch presented the PFS phenomenon to them, with all the published science and media accounts, we COULD persuade and finance sending multiple blood samples for testing. This should be done immediately.[/size]

Likewise, practically speaking, it behooves us to look into serious, scientifically-backed means of expelling pharmaceuticals. At the top of my short list (longer outline of ideas in the attached Toxicology Study) are: plasmapheresis, hemodialysis, IR Sauna, Bile Acid Sequestrants, Zeolite, etc. We’re talking liver, kidneys, colon/bile acids, sweat, maybe lymphatic drainage??

[Size=4]One thing I need help on is learning if finasteride is protein bound (suggesting plasmapheresis) vs. having a low molecular weight (suggesting hemodialysis).[/size]

This is just a theory – but one that I feel deserves to be looked at seriously by individuals talking to their practitioners, by individuals exploring potential treatments, and by the research community at large. This is too big, too simple and obvious to rule out. Even respected endocrinologists I’ve spoken with admit that it IS a possibility. Many drugs, many compounds are known to stay in humans for a LONG time after cessation. Finasteride is a prime suspect for this phenomenon if you ask me. READ THE DAMN PAPER I LINKED TO AT THE BOTTOM!

I hope someone finds this interesting and useful and inspiring. I have not even bothered looking around to see if Venceremos has shared the details of his story yet or if I’ve posted something redundant, but here it is, anyway. Hope this is our year!

*From attached Toxicology Study (please take the time to download and read this important paper):
[i]Some bile-excreted xenobiotics that are surface active, or which possess structural or behavioral prop- erties similar to endogenous bile acids, however, may have slower elimination kinetics and remain persistent in the body due to enterohepatic recirculation (EHC).31

The EHC is a normal physiological re-absorption mechanism for recycling bile acids and acts as a means to conserve required biological compounds; this mechanism, however, can act as a hindrance to elimination of some toxicants. After hepatic process- ing, delivery of toxicant compounds into bile with subsequent excretion into the intestine accounts for much elimination. In addition, some compounds appear to be delivered directly to the lumen of the intestine by exfoliation of the epithelium or exudation across the mucosa.30 Unconjugated compounds released into the gastrointestinal (GI) tract as well as conjugated toxicants freed by the action of enteric micro-organisms, however, become available to be re-absorbed and return to the liver through the EHC. Consequently, the cycle of excretion and re- absorption commences over and over again. The net result is that the process of recycling toxicants results in (i) repeated elimination by the liver thus consuming energy and nutrients, (ii) it severely prolongs the half- life of involved toxicant compounds, and (iii) it increases the potential health risk because of retained xenobiotics and persistent exposure. [/i]
Human & Experimental Toxicology.pdf (289 KB)

so what is the treatment. I think blood exchange?Maybe our livers are compromised we should donate blood and also take some blood.

could make sense. it definitely has been in the back of my head with all the methylation issues that people may be having. if methylation doesn’t work, toxins don’t get out. what’s saying finasteride didn’t get out either?

but the question is, is this possible to test this? also, how can we get finasteride out? IHP besides niastin, he was on collidoal silver, perhaps that could be a way to get it out? i’ll try to search into pharmacetical detoxes.

iodine occupies the thyroid receptors, i read a post randomly somewhere online that said finasteride contains high amounts of bromide (i really could not tell you if this is true or what this is has to do with) and it could be occupying the thyroid receptor. this made me think the random iodine or thyroid recoveries had warrant.

Ok but so what…even if we take the premise that its still in our system…why did we experience (a) persistent sexual dysfunction some of which is not even on the black label warnings and (2) why the hormonal crash. Not saying its a bad premise at all, but we may be putting the cart before the horse

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my dht is very high, if finasteride was still in me it would be very low, wouldn’t it?

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Aren’t there studies that like 99% of it comes out? And then of course the DHT levels definitely do rise after stoping the drug. What about the molecules that bound to 5ar2? What happened to the 5ar2-finasteride complex? Perhaps it has deposited in our body.

Fanjeera, could you please post any such study.

My DHT never returned unassisted. It’s been chronically low, right at the bottom of the range.

But DHT is just one casualty of inhibiting 5AR2…allopregnanolone and the whole chain of hormones are affected.

I’d like to see my hormones tested while on Nystatin, as that’s the main thing that’s ever helped me.

There are tons of those which show the DHT levels returning. That should be proof enough. What happens in the brain, may be different, though. Perhaps it accumulates there and inhibits allopregnanolone synhesis forever.
If it’s in the range, why worry? Do you know it was higher before?
60% of the 1 mg of fin absorbs. 90% of that is bound to plasma proteins. If I’m not mistaken that part is not able to cross the BBB at all and is inactive.

My doctor told me after I quit propecia it would take 6 months to leave my system. Wonder exactly what he meant by that? Traces of it in my system or it’s effects lingering. He always checked my liver but assumed my high bilirubin was due to Gilbert’s Syndrome.

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My doctor told me something like that or a year also. I have seen studies about that kind of time. I think the question here is only about the 5ar2-finasteride complex, as finasteride is a irreversible inhibitor. Why shouldn’t the rest come out? There are studies about half lives, the drug’s metabolism and its detection in the faeces and urine. Most of it definitely is coming out.
So start searching “finasteride 5ar2 complex” or something like that and lets study stuff!
And the question is not whether it’s still inhibiting the enzyme. It definitely is not, because the DHT comes back online, but perhaps the complex is causing other problems. And maybe it’s still inhibiting the brain allopregnanolone, because there’s not much proof about allopregnanolone coming back. Though, it probably does, because rats get their neurogenesis back when they don’t get fin anymore. Why not the same in humans?

I have been thinking about this theory for a while as well. Maybe our livers dont metabolize finasteride and its circulating in our bodies indefinately. I think this issue should be priority and would not be too hard to solve…

We are all different. Some of us have been hit really bad sexually (me), and have perpetually low DHT. Others have sexual function but no libido. Others suffer from worse cognitive fog. Some got hit with just a few doses. Some took finasteride for a long time, and the demise was more gradual (me).

Think in terms of each individual’s capacity to digest finasteride, and each individual’s reaction to inhibited 5AR, not just DHT.

It’s really astounding to me…an antibiotic can be in someone’s system 1.5 years later. After only 2 doses!

And we KNOW…it’s a published scientific study…that finasteride impedes its own metabolism.

Given these two facts, I would absolutely put testing for this possibility at the top of the PFS foundation and PFS suffering community and PFS researcher list. Let’s just rule it out.

is there any lab that can test blood for the presence of fin (Dihydro-Finasteride) or it’s metabolites?

There is one scientific team that has mapped the finasteride molecule. It would take an organized, diplomatic, credible, and possible financial approach to have it done. But it can be done. I’m trying to figure out what I can do behind the scenes; I have not been approached by anyone high up in the forum or heard anything from the foundation regarding this. I just really think it should be ruled out. If we know drugs can persist after a really long time, and we know that finasteride specifically impedes its own metabolism, why not just rule this out before jumping to more complex theories?

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I agree with and support your point. I’m not sure it can be completely ruled out though, if it crossed the BBB and imbedded in the tissue but isn’t being metabolized, there’s no real way to test for it until someone dies and their brain is donated, but blood/tissue testing is a good idea.

Do you have more info on the test vene used to identify the antibiotics? It seems as if Merck identified the half life of the drug, or their supposed half life number, the the technology to test for
it should be available…

This has been discussed before. It wouldnt explain anything. viewtopic.php?f=27&t=4003 Testing for Finasteride must be available if anyone will search enough. Little bit ironic that the nystatin/fungal prostatitis/leaky gut/candida guy who says men in white coats cant help - now demands doctors help!

There is a test for the Finasteride metabolising CYP3A4 enzyme here by the way: nicholsinstitute.com/TestDet … TestID=254 Anyone serious about this idea needs to test this surely?

This is also interesting viewtopic.php?f=27&t=6993&hilit=dutaseride#p61033

It can explain why some people had a sucsses with fasting, because it’s clean the body and the blood.

Can someone provide context for this test? What exactly does this show, how can one discuss this w/ their doc?

I’m out of the loop – was dutasteride really found in a deceased PFS victim?

Dutasteride has been found to induce genetic changes. It’s likely finasteride does the same.

"Dutasteride (Avodart), a drug used to treat benign prostatic hyperplasia, may also prevent the development of prostate cancer by inducing genetic changes at the cellular level…

Gene expression profiling was performed, finding 32 unique genes that were upregulated by treatment with dutasteride and 98 genes that were down regulated.
"

medpagetoday.com/MeetingCove … state/5119

eta: also interesting

“She said that IGEBP3, which appears to be upregulated by dutasteride, promotes apoptosis and inhibits cell proliferation.

Fin inhibits this enzyme which metabolises it. If the enzyme remains inhibited, then fin isn’t excreted from the blood system, but this tells us nothing about what happens behind the BBB unfortunately.

You can deduct from Paximperia’s thread that dustaride was still in his system with the dates he stopped taking it, the half life of dustaride (5 weeks) and the date he died.