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!
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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?
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This is also interesting viewtopic.php?f=27&t=6993&hilit=dutaseride#p61033
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It can explain why some people had a sucsses with fasting, because it’s clean the body and the blood.
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Can someone provide context for this test? What exactly does this show, how can one discuss this w/ their doc?
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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…
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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.
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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.
Let’s start from basic pharmacological knowledge first. Can anybody find what happens with an irreversible inhibitor in the body? It makes a covalent bond with the enzyme and then what happens? Is it forever? The cells definitely produce new enzymes all the time and the normal function of endogenous hormones returns. The question is, can the accumulating 5ar2-finasteride cause any new kind of problems. Can it even get out of cells? Probably not, so a biopsy is needed and a blood check isn’t enough.
Damn, it´s like basic pharmacodynamics, but I can’t find any info about it…
If drug pooling has occurred (theoretically/practically plausible), the end problem extends beyond that.
Death of two subjects due to imipramine and desipramine metabolite accumulation during chronic therapy: a review of the literature and possible mechanisms.
Swanson JR, Jones GR, Krasselt W, Denmark LN, Ratti F.
Source
Pathology Department, Oregon Health Sciences University, Portland, USA.
Abstract
In two unrelated cases, a 7-year-old boy and a 21-year-old woman died suddenly while receiving chronic imipramine therapy. In the boy, concentrations of imipramine were: Left femoral blood 0.5 mg/L, right femoral blood 1.2 mg/L, aorta blood 1.0 mg/L, liver 68 mg/Kg, and for the active metabolite, desipramine, left femoral blood 6.7 mg/L, right femoral blood 9.9 mg/L, aorta blood 8.7 mg/L, liver 400 mg/Kg. In the woman, the imipramine concentrations were: Femoral blood 0.6 mg/L, liver 37 mg/Kg, and of the active metabolite, desipramine, femoral blood 3.74 mg/L, liver 261 mg/Kg. In both cases, the scene investigation strongly indicated that neither individual had ingested an acute overdose. The very high ratios of desmethyl metabolite to parent drug are consistent with this observation. Impaired metabolism due to a genetically determined “slow metabolizer” phenotype of cytochrome CYP2D6, and/or concurrent therapy with phenothiazines, is suggested as a possible mechanism for the apparent fatal accumulation of these tricyclic antidepressants.
So there’s a variance between levels of the drug depending on where the blood is taken from? Anybody with background have comments if the 6.7-9.9 mg/L variance is significant? The liver concentration of the child is shocking. Something that’s generally assumed (I believe) is that the blood concentrations are relatively even throughout the body, however in this case it’s 33% higher on one side.
CYP3A4 is the enzyme that metabolises Finasteride.
Its actually the induction (increase) of the CYP3A4 enzyme that will inhibit 5a-Reductase and cause hypogonadism and hypocortisolism symptoms see: ncbi.nlm.nih.gov/pubmed/23162091 (something I predicted 2 years ago by the way). This exactly matches the symptoms and hormone/urine/blood tests of a severe case of Post-Finasteride Syndrome like nothing else.
Although there is no reason I can think of for CYP3A4 to work overtime.
But DHT levels return. We can’t be talking of a forever 5ar2 inhibition. It’s not happening.
Well, its all a matter of looking for something similar in the literature. This is clearly worth mentioning in regards to CYP3A4, the urine metabolite (& neurosteroid) results and the symptoms. It might also be worth reading along with this study that shows DHT remains even with increased androgen metabolism: ncbi.nlm.nih.gov/pmc/articles/PMC2488233/.
(then compare this to your ‘stress is causing all our symptoms’ idea viewtopic.php?f=27&t=7388 !)
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But seriously,
What would you expect to happen if CYP3A4 wasnt working? Wouldnt this be obvious? Why would this cause the symptoms?
(Or if Fin or dihydrofinasteride is ‘stuck’ in 5aR? Why would this happen? Why would this cause symptoms?)
The elephant in the room that we have to deal with first before any other question is how are we going to do this?
I totally agree that this is thing that has and MUST be ruled out through tests/research and we preferably have to prioritize it to top as well. Has Mew, awor or anyone responded to this yet? It’s hard to imagine anyone else with the resources to do this now. I’d gladly participate if possible, sending a serum tube in ice shouldn’t be that difficult innit?
DHT did not return for me. And I’m one of the most severe loss of brain-to-penis connection/sexual dysfunction/E.D. PFS cases out there.
Interesting discussion on the CYP3A4 Enzyme here:
anabolicminds.com/forum/male-ant … zymes.html
Building on the themes of Phase I and II Liver Detox from the above as well as Methylation, MTHFR Genetic Defect discussion by Chris Kresser*:
chriskresser.com/paleo-diet-chal … x-capacity
Another Phase I and II Liver Detox explanation:
vrp.com/detoxification/phase … x-pathways
[Size=4]*disclaimer: yes, he’s plugging his own line of supplements now, after years of putting out free research analysis[/size]
You’ve got before and after DHT test?
Has Melcangi said anything about Finasteride still being inside us ?
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