Yes it is. Like I said in my post I focused my discussion with the scientists on the androgen receptor theory, because I believe that it does the best job at explaining what happened to us. Having said that, we also touched the possibility of 5AR not functioning correctly anymore. At first sight, it seems to be the obvious thing to look at considering that finasteride inhibits 5AR. More on that later.
Unfortunately, all of our theories will remain such until we can prove something in a lab.
You’re right, and I should have stressed that more in my post. Three scientists told me this as well. Our bodies are incredible machines, which can compensate for and repair just about anything. The point I was trying to get across was this: If we are hoping that if everybody chips in 50 bucks and we hire a scientist to solve our problem, we’ll most likely be disappointed.
The power of healing is within us. Deceivingly simple ideas like juicing/diet/herbs/lifestyle etc. can help promote these powers. Believing in ourselves and giving our bodies the time and support they need seems to be a more promising route to me.
This does not mean that we must give up all hope in science. All of the scientists confirmed to me that developments can all of the sudden go very quickly after perhaps years of achieving no results. It’s not a linear business where input leads to continuous output. One of the areas I have been looking into is full genome sequencing. This technology basically lets us analyze the full 3 billion base pairs of the human genome (which includes dna and tons of epigenetic information). This allows for a genetic comparison between “us” and the “other” guys (who don’t have a problem with finasteride), without knowing where to start looking. Once we find out what “sticks out” in our genetic information, scientists could then determine what functions in our body are encoded by these genes - basically attacking the problem from the other end. Currently, such tests cost around $100’000 a pop. This cost is expected to be reduced to under 10K within the next couple of years (< 5 years). We’re in the midst of a molecular tool revolution at the moment.
The answer to this is likely to be quite simple. Even though we are all suffering from the same basic problem, the variation even amongst us is probably still relatively large. In other words, we are not all the same. It is obvious from reading the member stories that we are also not all affected to the same degree. The less affected amongst us are primarily suffering from some degree of ED. I can very well imagine that this group has got sufficient remaining androgen sensitivity to allow for TRT to improve their symptoms. My sensitivity is probably pretty close to zero. But even I sometimes get a little benefit from TRT (sometimes I also get the contrary). In other words, androgen insensitivity has many shades of gray, it’s not all simply black or white, on or off. If you read through the AIS literature, you will notice this as well (Btw. I am NOT saying that we have AIS, this is just an analogy to a remotely similar problem)
I had this testing done as well, except with normal skin tissue, but the results where the same. Let me quickly clarify what we mean by gene expression, receptors, etc. and how it all ties together (hi level):
Ligand (hormone /input) => Receptor (plug) => Signaling Path (machinery) => Gene Expression (output/androgenic action)
Sequencing the genetic code of the androgen receptor, in order to check it for known defects, does NOT tell us anything about what happens at the other end of the machinery. We even know that the receptor is functioning correctly in both cases (chams and me). BUT you can only tell if something is coming out the other end by quantifying the output (gene expression). The scientists are telling me that it is in the machinery (signaling path) that things can easily go wrong (remodeling of signaling paths, etc.). Various mechanisms of gene regulation can play a role here (as described in my last post).
While on the subject, let me use this model to explain why my specialists and myself believe that the problem is somewhere “downstream” from the receptor. Let’s run through what we know about each variable in the equation:
Let’s start with the output: In the most serious cases we’ve got massive penile shrinkage and massive muscle wasting. These are both hallmark androgen dependent tissues. Then we’ve got ED, loss of aggressivity, prostate, etc. Also well know to be androgen dependent. So we are clearly missing out on androgenic action. In other words we are lacking “output” (gene expression).
Ligand/Hormone: Some of us have a lot, some too little. It doesn’t matter. In the best case you can inject an insane amount of Testosterone and get some improvement. In the worst case the same amount won’t do anything. In any case I am still waiting to hear from a guy that has 100% solved the problem through TRT. So it can’t be the hormones.
What about DHT, maybe we’ve got too little or from the wrong enzyme or whatever. Permanent damage to 5AR is actually not a bad theory. But it has a major shortcoming that pretty much rule it out: It doesn’t explain muscle wasting. DHT is not required to build or maintain muscle mass.
This is demonstrated in male pseudohermaphroditism due to congenital 5-AR deficiency. When puberty occurs, the testosterone levels of these individuals raise normally, although their DHT levels remain very low. Despite this, their musculature develops normally like that of other male adults. There are about 3-4 other arguments which further support this and are scientifically backed (joe.endocrinology-journals.org/c … t/170/1/27).
If this is not convincing enough, try supplementing it (I have).
So in my opinion and with current medical knowledge, we can pretty much rule out hormones. But what about all the other hormones? Well, I haven’t found any scientific litterature which explains why androgenic tissue dies because of a dis balance of other (non-androgenic) hormones. Maybe someone can correct me on this. What about hormones that could have a gene silencing effect (regulation) on the androgen receptor? That’s possible. But then we would be talking about something hitting the machinery. Or take a hormone like prolactin. You can explain ED with it, but not muscle wasting. The key is to find a theory which explains everything for everybody. It can’t just work for isolated symptoms or for certain members. In other words, a lot of things can potentially explain ED. If you try combining ED, depression, muscle wasting and penile shrinkage (just to name a few), the number of options gets real small real quick.
Receptor: As stated above, Chams and me had them tested. They work. This for me is sufficient evidence to rule out the receptors.
What we have got left is the machinery. The piece in between that is still partially a scientific mystery. A machine 1000 times more complicated than a missile guidance system. What are the odds?
Just imagine if a scientist finds a solid explanation to our problem one day. All the theories collapse in themselves. What are we going to talk about then in this forum? It’s going to get real boring around here at some point! 
I am hoping to start covering the nutritional side of things with a scientist/doctor in about 1-2 months. I’ll report back on this interesting subject as soon as I find out more.
Keep up hope!
