Yes, that’s the main issue I suspect.
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Might there just be a chance that what’s happened here happens in the rats?
By which I mean, say you manage to induce PFS in rats and can reliably test for it. You throw all the supposed cures at the rats in rat-doses and then none of them get cured. Then one of them gets cured with Tribulus, then you never replicate that again - no more rats are fixed from Tribulus. Then in a month repeating everything over and over Gingko cures another one, but doesn’t cure any others, and didn’t cure any before that one. Then one of your other rats from the first batch you didn’t euthanise just gets better where none of the others do, again even if you can even reliably diagnose PFS and PFS cured in a rat.
If I just took a massive dump on the idea I’m sorry for it. But it does seem like the same circle we’ve tried here before on (VERY willing) human guinea-pigs desperate to get back to where they were, who can reliably report symptoms too. We had Solvepfs and other forums… lots of protocols and nothing we could replicate reliably. Don’t we think it’d just be the same thing except more work in determining what a rat’s feeling?
(EDIT - also when I say above I am sorry then I do mean it, if I’m stomping on hopes there. I think (probably dangerously ofc) that human self-experimentation is the way, which I’ll carry on with I must say. I am certain given the many years of PFS that there’s not one-size cure for it. But where to look for a fix for the 2+ types of PFS then who knows. Where DO we start even? How you respond to masturbation? To increasing or reducing androgens? There’s not even one thing that PFS seems to be as far as I’ve read.)
This is a possible eventuality. But it’s unlikely if the same weight-adjusted dosage is given. Who knows, it’s all speculation.
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The difference is that it’s a controlled environment and you can test 100s of rats potentially.
- Can rats get PFS?
- How can you reliably tell if a rat has PFS?
- How many rats are needed to get a decent number of PFS rats? I. E. do you need potentially 1000s of rats for 10 PFS rats?
- How different do rats react to humans when it comes to PFS and protocols?
- How likely is it that one will find a cure? I. E. is shooting in the dark worth the investment, even if it’s a much more controlled environment than a forum.
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Yes definitely makes sense on all.
I’d also add in the maddening confusion of some things which might cure one rat make another one worse. And also how you’d find out if a rat is feeling worse or not. But who knows, there might be something consistent. You’d definitely not run out of protocols to try!
It hasn’t happened so there’s little point discussing the hypothetical.
If I were a rat, researchers would be able to tell I have PFS very easily…
You throw the rats a piece of rope and the ones that try to hang themselves will likely have PFS. The rest will simply sit around watching.
If we knew which genes led to PFS that would be much easier. Melcangi identified one gene to do with Methylation.
There maybe some obvious signs if their DHT lowered assuming they have DHT.
At what point do we stop being victims of PFS and start doing something to take back our lives?
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Lol.
And phase 0 of this study, of course, should be to directly establish (i.e. in a placebo controlled study) that PFS exists in the first place, which believe it or not, has not been done in animal studies so far, to my knowledge. It is as simple as giving 100 matched pairs of rats a single dose of finasteride vs. placebo and then counting how many in each condition permanently lost their sexual function. Has any study in history been easier and more straightforward than this?
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Rat as an animal model for male erectile function evaluation in sexual medicine research.
Animal models have contributed, to a great extent, to our understanding and advancement in the field of sexual medicine. Many current medical and surgical therapies in sexual medicine are the direct result of the development of such animal models.
So we can determine if a rat gets ED from taking Propecia.
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Also, once you have rats with PFS it will be relatively simple to test the heck out of them to see what’s wrong with them. Unlike previous studies, you are only going to test rats with PFS, not the whole group who took finasteride, which is going to give a much more valid signal of the relevant abnormalities.
I’m on-side @Sibelio. Why is this approach not being advocated by the foundation? It is extremely low cost and high reward.
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This approach assumes that it would be easy to “make” an animal model. Unfortunately, this central assumption is wrong. If we had that model, we would be half there in terms of understanding this problem.
Specifically, what we need is a disease model of PFS. We know from humans that only a small percentage of those that consume finasteride get PFS. There are some predisposing factors that make us different from those that can happily use finasteride and not get hurt. Those are either genetic and/or epigenetic. Some get PFS after only a a few pills, others can take it for a decade before PFS strikes. There again, we need to understand the underlying difference between those extremes.
Only with that knowledge can we hope to engineer a disease model that will get “real” PFS when fed finasteride for a short while.
A good disease (animal) model is the holy grail of medical research. To reach that, we need to understand what the genetic driving factors are behind PFS. A good start to this would be if more patients would participate in our 23andMe project.
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Thanks for the reply. Just to clarify, are you saying that it would not be possible to tell if a rat has PFS?
In your estimation roughly, how many steps would you say are required before we get to that point?
Suppose Baylor study if they really do well and give us what it was designed for, is 1 part
Then the 23 and me test is another.
In your estimation, how many parts might be required before we get a disease model?
It probably isn’t easy to tell if a rat has pfs, but that is not what I wrote. My point was that you can’t just feed a rat finasteride and then assume it has biological equivalent of pfs (not just depressive behavior, or whatever). First, we don’t even know exactly what pfs is at a molecular level, and second if we did, one would need to genetically predispose the animal to be susceptible to get pfs when exposed to fin.
Idk, there are still too many variables open at this point. If we get really lucky, then 23andMe data might reveal some SNPs of interest, which would help us pinpoint some genes to investigate. And then if Baylor hits it out of the park, their data, combined with the 23andMe data just might reveal something interesting. My guess would be that these efforts will show us where we need to focus on next. At that point I am of the opinion that we need to go commercial as opposed to just working with academics. The academic route is just too slow. We need the data faster, then the academics can publish whenever they feel like it - we won’t care.
In any case, I doubt that we will have a chance to find anything before we have at least double the 23andMe genomes compared to what has been submitted, that means at least another 50, better 100. It would be great if all the survey takers also provided their genomes, that would be really helpful.
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Guys we need another 100 participants at least but the more we have the better.
We need a big push from this community. Looking at the survey results so far we can determine that 75% of participants have a tertiary education.
So we are looking at University students and graduates as majors users of Propecia.
We have our target audience!
All we need to do is reach out and start emailing.
That begins with emailing all your friends on social media and asking them to forward your message. Those of you who are young and have friends in Uni or have graduated have access to the people we need.
We are looking at an age group between 23 and 38 years old as the main catchment.
This is what you can send.
If anyone is taking Propecia please read this story. Merck has hidden the drug risks of Propecia which has already been linked to multiple suicides and over 15,000 patients reporting serious on going side effects.
A US Judge has allowed Merck to continue hiding the serious side effects of its drug Propecia from the general public.
For anyone taking Propecia you have no idea what damage this drug could be doing to your body. You need to ask yourself why would a reputable drug company hide the serious side effects of one of its drugs and who does that benefit?
Reuter’s has now asked for the release of the secret Propecia papers.
This is not the first time one of Mercks drugs has been linked to concerns about patient safety.
In 2004 Merck had to recall its popular arthritis drug from the market Vioxx which was linked to 140,000 heart attacks that resulted in approximately 60,000 deaths.