JVK:Originally Posted by jvkohl
You're confusing a few things here.
I've
never suggested that using human VNO affinity is known to be a reasonable approach.
In fact, I've stated
twice in this very thread that it hasn't been shown to be valid.
On the other hand, it also can't be ruled
out UNTIL we verify that the genes are not being expressed there and there are no receptors.
Has that been
shown? I haven't seen that research. If you know of such a paper, please cite it so I can read it.
The
point I was making is simply that there is some evidence, in Berliner's work, that he is finding something by
researching VNO affinity. The choices are:
a) He was finding out something useful.
This explains why
androstadienone had the highest affinity in males but not females in his experiments and why it was found to
actually be a pheromone.
b) He was getting random results that had nothing to do with actual
pheromone/receptor affinity.
In this case, it's pure dumb luck that androstadienone showed up as having the
highest affinity in males but not females, and it's also random chance that produced the sexual dimorphism he
found.
c) He fabricated the results.
This would mean that it was known in advance that
androstadienone was a pheromone. Was it? Do you have any citation that shows this was the case?
I am trying
to be logical about the information that we do have, and I am hoping for a response which actually and specifically
addresses the issues I'm raising, rather than a dismissal.
Once again, I'm NOT saying that VNO affinity is
proof of anything, but that there appears to be evidence that something is going on there, EVEN THOUGH there's no
evidence that the VNO produces any brain responses in humans.
Bookmarks