MHC difference exactly predicts female faithfulness

[xvs]

http://www.newscientisttech.com/article.ns?id=dn10847&feedId=online-news_rss20

A very

interesting finding:

The fraction of MHC genes shared directly correlated to the woman's number of

adulterous partners – if the man and woman had 50% of the MHC genes in common, the women had a 50% chance of

cheating with another man, on average.

And this:

“We’re fairly certain that all of this

revolves around scent,” she adds. “Now all we have to do is track down the specific chemical cocktail responsible

for all the behaviours we are seeing.”

[jvkohl]

http://www.newscientisttech.com/article.ns?id=dn10847&feedId=online-news_rss20
A very

interesting finding:


Good catch xvs. I waited to receive and read my reprint of the actual

article before commenting.

In the journal article, the authors conclude that "MHC sharing negatively predicts

women’s sexual responsivity to and sexual satisfaction with partners." More sharing correlates with greater

attraction to other men, especially when the women are most fertile. "These effects may be mediated by

scent..."

The fertility-scent link suggests that estradiol may enhance the ability to detect and

differentiate among MHC/HLA -related pheromones that are shed in skin cells. These skin-cell pheromones are

processed by the main olfactory system, again, with no human VNO

involvement.

JVK

[xvs]

You rightly make the point that the

VNO is not responsible for pheromone actions in humans, but this doesn't mean that the receptors found in the VNO

are not pheromone receptors.

The experiments I'm aware of (unfortulately I don't have the citations handy)

which explain what's going on with the VNO in humans are the following, which were cited by Dr. Ivanka Savik in a

lecture I attended last year:

- In the first experiment, the VNO was blocked in a number of subjects, and

they still showed pheromone responses when exposed to pheromones (I think via the PET scans she usually

uses).

- In the second experiment, the olfactory epithelium (where the receptors are) was blocked but the VNO

was left unblocked. No pheromone responses were shown during pheromone exposure.

- In the third experiment,

people who had natural blockage of the olfactory epithelium and so suffered from anosmia (lack of ability to smell)

were tested. They also exhibited no pheromone response during exposure.

The conclusion was that pheromone

responses have migrated in humans from the VNO to the olfactory epithelium.

In a related series of

experiements, it was shown that RNA encoding pheromone receptor molecules was found in human olfactory epithelial

cells. I believe this was determined through annealing with primate or other mammalian pheromone receptor RNA

obtained from VNOs of those animals.

These experiments showed that the pheromone receptors were being

produced by the human epithelial cells, as could have been expected from the previously mentioned findings.



What was NOT tested to my knowledge was whether human VNO cells still ALSO produce pheromone receptors.



It's been determined with good assurance from the first set of experiments that the VNO is no longer

functioning in humans and that its functions have been taken over by the olfactory epithelium, but it's not known

whether the human VNO has stopped producing the pheromone receptors or not.

So it is possible (although

certainly not proven) that human VNO receptor affinity COULD be indicative of pheromonal activity.

What's

lacking is a study which determines whether the same pheromone receptors now present in the human olfactory

epithelium are still present in the human VNO.

[belgareth]

Perhaps it was stated somehwere

and I missed it but which pheromones did they use for the experiments? I do not claim to know if the VNO works or

not but think that if it does it could be specific to a certain set of pheromones. It should be eliminated, if

possible.

[Tiger4]

I would like to know if MHC

differences are correlated at all with racial differences. Presumably it is true because racial differences came

about due to geographical differences and people from different geographical regions tend to have different

immunities as they have to deal with different climates, plants and food.

[jvkohl]

It's been determined with good assurance from the first set of experiments that the VNO

is no longer functioning in humans and that its functions have been taken over by the olfactory epithelium, but

it's not known whether the human VNO has stopped producing the pheromone receptors or

not.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list

_uids=16733333&query_hl=7&itool=pubmed_docsum

"In humans... all structures except the vomeronasal duct

undergo regression... Histochemically, it is lined with a remarkable pseudostratified epithelium, the nature and

significance of which are still unclear."

From what I've heard at conference presentations and from what

I've read in the "proof" copy of the paper cited above, there appears to be no reason to look further for human VNO

receptors. If, as indicated by the abstract excerpts, all that's left of the human VNO is a duct containing

"pseudostratified epithelium" (e.g., without nerve cells that might contain receptors that could allow signal

transduction to the CNS), it becomes even harder to imagine why anyone would continue to propose that there are any

human pheromones that function via the human VNO.

Belgareth, I think that this is a "wrap" so far as any

human VNO debate is concerned. Any evidence not already reviewed by these and many other highly esteemed authorities

would have to re-establish its presence as something other than a vestigial duct, somehow innervate it with nerve

cells, and find genes that code for the pheromone receptors on the nerve cells.




JVK

[belgareth]

I'm not debating, I am asking

questions for my own knowledge. You didn't answer the question other than telling me why it shouldn't be done.

That's fine as far as it goes but I like to check assumptions, that what I was taught was good science.

[jvkohl]

I would like to know

if MHC differences are correlated at all with racial differences.

But it's not politically correct

to discuss racial differences, let alone their possible biological basis.


Presumably it is

true because racial differences came about due to geographical differences and people from different geographical

regions tend to have different immunities as they have to deal with different climates, plants and

food.

On the other hand, it's hard to argue against this "logic."

JVK
.com

[jvkohl]

I'm not debating,

I am asking questions for my own knowledge. You didn't answer the question other than telling me why it shouldn't

be done. That's fine as far as it goes but I like to check assumptions, that what I was taught was good

science.

I know that you're not debating the issues. And I'm only using the existing literature to

answer questions on why no further research is being done. I'm not saying it shouldn't be done, just that there is

now a rather obvious "dead end" to any career effort spent trying to find things that others repeatedly have shown

do not exist.

Granted, when I first began looking for information on human pheromones in the early 80's, I

was repeatedly told they didn't exist. The difference between then and now is that few people had bothered to look

for evidence that human pheromones do exist.

But there is also a difference between the early 90's and now

with regard to evidence for the human VNO. Initial reports said it existed, but those reports inspired others to

look for evidence that it exists. They've looked, and can't find any evidence that it exists, either in the

genetics (no genes that code for receptors), in the neuroanatomy (no tissue containing nerve cells), or in the

neuroendocrinology (no hormone response generated).

For most researchers, "three strikes and you're out"

would be the metaphorical reason not to bother further checking their assumptions that there is no human VNO. It is

also "good science" to know when to get out of the "game." We still produce pheromones and we still respond to them

with changes in hormones and behavior. But for most olfactory researchers, the VNO game is

over.

JVK

[platinumfox]

This is very interesting

stuff I wish there was a way to visually measure this on each on each woman that walks by.It would save alot of

trouble and money.

I am good at reading people and can tell by the womans eyes if they are permiscuous even

if they are in a committed relationship.Most have this "Im innocent" look in their eyes but are really messing

around and just devious....I dated one but now I can see that look in other women and just sympathize with the guy

she is pretending to have feelings for.Then there are some who just constantly have that look of sex in their

eyes.

[xvs]

Perhaps it was stated

somehwere and I missed it but which pheromones did they use for the experiments?

androstadienone was

used in Savik's experiments.

JVK:

I don't think you can rule out VNO affinity as being predictive

of pheromone effect, even if the neural connection between the VNO and the brain is no longer present, and even if

it's been proven that (for some pheromones at least), the olfactory epithelium is what's active.

The

reasons for this are:

Berliner et al found all these different binding affinities in the VNO. So

SOMETHING was binding these compounds. That something is very likely a receptor.
The affinities were sexually

dimorphic. More evidence.
The compounds which were preferentially bound to male VNO were female pheromones

and vice versa.
One of the greatest affinities they found was androstandienone in females, and sure enough,

androstadienone turns out to have pheromone properties in tests on females. It also has pheromone properties in

homosexual but not heterosexual males, as shown in Savik's experments.


So to say that the human

VNO has no receptors is just not something borne out by the evidence. It has receptors, but they don't seem to be

conveying any information to the brain.

What we don't know is how well correlated VNO affinities are to

pheromone activity. And that's all we can say about it.

[belgareth]

Thanks, XVS. That answered my

question.

JVK,

Perhaps biological research is different fom the areas I am trained in, or my wife for that

matter. In both cases we were taught to cross all the T's and dot all the I's before any research can be called

complete. That means checking all the assumptions. Examples of situations where it wasn't done can be seen most

dramatically in the Tacoma Narrows Bridge and the two destroyed space shuttles. Admittedly, lives are not at stake

when it comes to pheromone research so it may be different there. However, failing to check those things would have

resulted in some red ink from any of my professors in college. In my professional life it is often the difference

between a two hour job and a twelve hour job. Failure to check assumptions has cost me a lot over the years.

[jvkohl]

Thanks, XVS. That

answered my question.

JVK,

Perhaps biological research is different fom the areas I am trained in...

Failure to check assumptions has cost me a lot over the years.

xvs,
Prefacing human VNO-related

findings with "Berliner et al found" incorporates the assumption that these findings, which have never been

replicated, are accurate and portrayed accurately.

Belgareth,
When others assert that what "Berliner et

al found" is highly unlikely for many different reasons, it starts to come down to who you believe. The human VNO

approach is the least consistent with the data from studies I've read.

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; 2) no tissue containing nerve cells; 3) no hormone response generated --would help to untangle

the mess. I don't know any other way to address the issues. There are at least 3 reasons not to include Berliner's

human VNO approach in the conceptualization of human pheromones, and no good reason to include it (for example,

replicated results might be a good reason). Since the majority of olfactory researchers I know do not incorporate

the human VNO approach, I'm willing to go with the assumption that, collectively, we know enough to proceed--as

Savic and many others have done--to forget about the human VNO, and find out more about what human pheromones do.



JVK

[Icehawk]

Ok so am I the only one here who

sees potential for a pre marriage screening and divorce use?

[jvkohl]

Ok so am I the only

one here who sees potential for a pre marriage screening and divorce use?

You may be. The fertility

clinic work-ups, or paternal genetic testing only come after-the-fact. All are related to the MHC, i.e., the Human

Leucocyte Antigen (HLA) locus of genes; its genetic influence on pheromones, and pheromone-associated human sexual

behavior.

JVK

[xvs]

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.

[jvkohl]

JVK:
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.

I didn't go back far enough to catch your

drift, sorry.



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.

I can recall only something

vague about pseudogenes--and they may have had nothing to do with human VNO receptors, though I've managed my

memory to think that this connection was made. Peter Mombaerts, perhaps or Richard Axel--I tried to find a

reference, but if the article is more than a few years old I don't always have a .pdf or print

copy.



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.

My partial point was that work from his group

has not been replicated and it is not likely to be. If ever it is, it will deserve more thorough

review.



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?



Option d. in a multiple choice format could well be "all of the above." However, something not yet

given much consideration is that androstadienone (and its sexually dimorphic VNO affinity) might be part of a

sequence of events that allows it to interact with responses to other parts of a pheromonal chain link fence. I'm

reluctant to speculate much further on this, because people are already plagerizing what I say here for their own

commercial interests, but you and a few others may see it coming.



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.

I don't mean to be dismissive; I recognize and value

your logic. But we have differences in our logic. Mine says to use a mammalian model--for all its worth. And it's

worth a lot more if we ignore the unlikely human VNO--at least for now, until more human VNO research is done, if

ever, which I doubt. And, to me, unpublished, anonymous, or unreplicatable research doesn't

count.



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.

What I'm trying to say is that because there's no evidence that the

human VNO produces any brain responses--yet there is evidence androstadienone does (despite human non-VNO delivery)

produce brain responses, focus should now be on these brain responses and how they are linked to behavior.



There has been too much focus on a non-existent (or perhaps just non-functional) organ (or vestigial pits)

for too long--and this focus is largely due to product marketing claims that are still being made. Savic, Lundstrom,

Laska, Sobel, and many others have moved on--and this is a good reason for you and I to move on also. These

researchers are not promoting any products. So even though I have commercial interests, it should be obvious that my

research interests go with the flow. I'm interested in what you will say once you read my forthcoming review (and I

hope you will do so--as it details much more than I could ever write here).

JVK

[xvs]

I'm interested in what

you will say once you read my forthcoming review (and I hope you will do so--as it details much more than I could

ever write here).

Your last review was great, so I'm looking forward to this one.

When will

it be out?

[jvkohl]

Your last review was

great, so I'm looking forward to this one.

When will it be out?

The journal article is cover

date is 2006 but not yet available--sometime soon is all I know.

Here's the URL (which includes the

abstract):
http://www.haworthpress.com/store/Toc_views.asp?sid=BHPDKF23AUXU8G4E0XCM5PH7V06J8NPF&TOCName=J056

v18n04_TOC&desc=Volume%3A%2018%20Issue%3A%204

see: The Mind's Eyes: Human Pheromones, Neuroscience,

and Male Sexual Preferences Page Range: 313 - 369
James V. Kohl

As indicated by the page count (compared

to my Neuroendocrinology Letters review), it is much more inclusive/extensive.

JVK