Quote Originally Posted by jvkohl
xvs,
When the human

VNO approach is "mixed" into the data set, as xvs does when Savic's work (with no human VNO delivery system) is

added, the issues involved--and the assumptions that go with them--become a tangled mess.

I thought that-- 1)

No genes that code for receptors
JVK:

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.