The mechanism which we have found, combined with another (offsetting) mechanism, would be capable of explaining just about every aspect of our problem. Now we need to dig deeper. We are currently in the process of lining up all the prerequisites for the next round of investigations. The initial experiment basically confirmed that we are looking in the right place. In a next step, we will be zooming in on what we found, to understand as much as possible about the exact root cause molecular mechanisms involved. In other words, a key part of the hypothesis has been verified, but now we need to verify and understand the rest. I hope that we will be able to make a major announcement about the details of the next steps within the next two or so months. With the support and cooperation from all members of this forum, I promise you that 2012 will mark the biggest milestone ever in the scientific discovery of this problem. Stay tuned.
That’s nice to hear. Sorry if I’m repeating things but did I understood right: instead of releasing the results/numbers of the results for public/scientific scrutiny, you are going to use those results to and with two complimenting mechanimsm… to make the next study after those 2 to 4 months (to form a hypothesis)? So we probably won’t see the results of your first study before the second study is finished (into a scientific paper form) which would/could be…at the end of 2012? I can understand the reasons why you wouldn’t but I’d like to clear this out.
We all want to get moving as fast as possible with the experiments. I think that is in everybody’s interest. Finalizing a paper for publication unfortunately takes a lot of time. The initial time frame was too ambitious as it turns out. You may recall how long it took Irwig to get his paper published after doing the interviews, and there wasn’t even any lab work involved there.
As said, the first experiment helped us define the basic problem. Now we need to go into much more detail. This is only possible, because we now know where to look. From a time plan point of view, there is no benefit in waiting for the publication of the first results in order to start the second series of experiments. Like I said, we don’t want to loose any time. And no, the result will not be a hypothesis. One of the things we will be looking at in the next step is gene expression at a full genome level. In the best case, this will reveal a potential therapeutic target. In the worst case, it will provide us with more information about where to look next. The whole project will include other experiments as well, and we will tell you about those as soon as we are ready and have everything finalized and ready to go.
pretty damn exciting is you ask me. thanks guys.
This is very inspiring news thanks Awor. Please try to keep us all updated as much as you can good luck.
Awor,
we really owe you a lot for all your commitment and effort.
Hey Awor, thanks for everything. Where are these studies taking place again? Are you going to need more volunteers for the second set of experiments? And from your post, I understand that you WILL publish the first experiment but just after you start the 2nd one correct? So we could see the published study by this summer hopefully? This would be good to show doctors and get them thinking about possible treatments.
We will communicate the involved institutions and their locations as soon as all the agreements have been finalized.
Yes. The participation of patients will be absolutely critical to make this happen. We will be talking about substantially larger numbers then with the pilot study.
There is no reason at this point why the scientists would not publish. I can’t say anything about the date at this point.
The level of detail we have is not yet sufficient to provide information about therapeutic targets. That’s why we need to do the next research step in the first place. Root cause treatments, if they exist, will likely come from the research side and not from doctors. Practicing doctors, and I don’t mean this despectively, do their job by providing known solutions to patients for known problems. In our case, both don’t apply. In other words, the “seed” inputs regarding therapeutic targets and treatment strategies will probably have to come directly from the involved research organizations. If some sort of a baseline treatment can be established, then the treatment strategy can start to be multiplied (and optimized) by practicing doctors. Anything else seems unrealistic to me at this point.
awor in your opion is this curable including penis numbness based upon what u have seen?
Since Merck is pretty much evil as they come, is it safe to name the universities and locations of the studies? Maybe I am just paranoid.
I think its safe to say Merck would try hard to prevent these studies taking place as publishing research journals would provide evidence for the damage caused by their drug.
Awor, is the publication at least been submitted for publication and now its in the review stage?
If “root cause treatments” do not exist are we left with any options? Can you expand on that at all?
To add to boston’s question, is it possible that chronic prostatitis or other prostate problems serve as the root cause?
I’ll save you the wait: no.
The study was on tissue and DNA not the prostate.
Let’s see, how shall I answer that one without starting a flame war: 
First of all, the short answer is: No. I don’t really want to get into the question deeper than that because I don’t want to start a prostate theory battle here, and I frankly find talking about it a waste of time.
From the clinical presentation of this syndrome, it is clear to all of the scientists involved in the research, and even many reasonable thinking doctors, that we are having some sort of problem with AR signaling (often referred to as “androgen insensitivity” of sorts). What I mean by this is that the root cause of every single PFS symptom is somehow tied to a lack of androgenic action. Without even doing any research, this clearly points to some issue at the AR level or downstream thereof. As I have already mentioned in earlier posts, our initial pilot study has found a definite problem at the AR level, which basically confirms what we are seeing clinically. Given these results, we are not wondering anymore what possibly could be causing this, but rather are now focused on trying to understand the precise genes and epigenetic mechanisms involved in creating this persistent syndrome. This understanding is a prerequisite for thinking about cures and assessing curability.
No doubt, PFS has seriously messed up the lives of many people around here. Understandably, people are desperate for answers. We all want to understand what has happened to us and what we can do to get our lives back. The thought of living in this state is a scary one for many of us. It is human nature to try to come up with answers, even when there are none:
If you look at how theories come to life around this place, it is always the same story: Someone tries something, maybe based on a “hunch”, and has some degree of success with it. Invariably, this person will then try to cook up some wild, pseudo-scientific theory which supposedly explains why their therapy is “working”. Other sufferers then jump onto the band wagon and many will find that it doesn’t really work for them. The original self proclaimed “expert” will then come up with some further theory about why it may not be working for other users, and what has to be done to optimize the therapy. Despite further theorizing, the success rate remains low and some people move on to the next theory. And so it has been going on and on for years around in this forum. I am surprised that people aren’t getting sick of this by now. I do want to be clear about something though: I absolutely do support trial and error therapy attempts, as long as they are reasonably safe. But it would be sufficient if the “therapist” would just report: “Hey guys, therapy ABC has given me XYZ benefit”, with out getting into “…because of [some wild theory]”
Let me be very direct and clear about something else (I have said this many times before): PFS is a seriously complex, molecular level problem. If it weren’t so, it would have been solved by now. It is likely that the understanding of the involved mechanisms will represent a major milestone in the advance of medicine because it almost certainly will have implications way beyond only PFS. This should make it clear how complex this problem is and that there is absolutely no way that it can be understood without doing the scientific research. One can’t just cook up a theory and “guess” what the problem is. The only way forward is to validate each and every assumption or hypothesis made with experiments. Not a single non-research doctor has the knowledge and/or resources to perform these experiments. Needless to say, there is not one chance in this universe that any user from this forum can come up with the answer to this problem, as convinced of himself as he may be.
To wrap it up, I think the point has come where we should really start to take distance from all the user generated theories around here and start focusing all of our energy on real honest science. By honest I mean that there is no promise for a quick fix, and maybe there isn’t any fix. But we need to go down the path of real science to find out the real truth. At the same time, let’s not refrain from trying out (safe) therapies. Who knows, maybe someone will land a lucky punch. Just lets have some more humbleness and not pretend that we know it all.
What has been done to us through means devised by science, through reason should also be remedied by science. In other words I am certain there is a means to fix it, though it may not be readily known or even yet attainable.
Sir,
You could’nt of put it better.
I know the organization and planning takes a long time, but is there anything we can do to speed up the process? For example, will the 2nd study need penile skin biopsies? Is there a way to get the research team to start collecting these now?
Also, I’m curious about the difference in symptoms. For example, what causes the difference in severity of insensitivity, weak erections, low libido, shrinkage, etc? Is it how much the signal has been down regulated (like on a scale of 1-10)? The impression I got was that the AR signaling got turned off like a switch (all or nothing). Do you know the reasoning behind these different degrees of severity?