15. Human Sexual Behavior I

[MUSIC PLAYING] Stanford University. Is this on? Yes. Well, congratulations. Everybody has survived
the midterm including the TAs so far, who
recently have been let out of their entombment
with thousands of pages of exam pages. So those are rolling along,
and everybody is still awake so that’s good. OK. So we have now
officially entered the second half of the course. And organizational
things– readings will now be read hopefully. OK. So that’s not useful. Books. Books. Now is a good time to
actually go and start reading those books. And again, if you are not
up to all of both of them, some recommend the
chapters have come along. Pay attention to those. And again, a subset of you– may
not know it yet, but about 25% of you will have your life
transformed by that chaos book, whereas 25% will resent
the purchase price and my forcing you to do this. Also, another major,
major transition here, which is, as far as I can
tell so far, I have run out of steam turning
the extended notes into actual expository
writing, so they’re just going to take the form of really
poorly organized outlines. So that happens. OK. What else? What we now
transition to is going to be our strategy for the
rest of our course, which is to look at various subjects. And coming down the pike after
the lectures today and Friday on sexual behavior will be
aggression, competition, cooperation, empathy,
potentially language use, schizophrenia. Somewhere in there,
there is going to be a week or so
on that chaos stuff. But for all of
these subjects, we are now going to follow
the general strategy. We will start off looking
at what the behavior is. And what we’re going
to try to do there, in addition to looking at in
lots of different species, is to be as objective as
any good old ethologist in considering the
fixed action patterns of the particular behavior. That established, with the
promise that, in lots of cases, what we think comprise
some of these behaviors turn out not to be the case. That established,
what we will start is our inexorable march to
the left, the timeline that constitutes everything
we learn now, stepping back and saying, OK. One millisecond before
that behavior occurred, what was going on in the brain? What parts of the brain? What neurotransmitters? All of that. Stepping back before that, a
second before, a minute before, whatever, what was
it in the environment that triggered the brain
to produce that behavior? What was the acute
releasing stimulus? Stepping back, what do
hormone levels that hour, that day, some such
time span of that, what acute hormonal exposure
had to do with sensitizing you to the environmental
stimulus which released the nervous system
into generating the behavior. Marching all the way back, throw
in culture some place or other. Perinatal effects, early
developmental hormonal stuff, eventually considering what do
the genetics of the individual, of the population, of
the species– evolution kicking in there
some place or other– what do all of these things
and something having to do with ecology thrown in
there just for good measure. Working our way back
in each of these cases, understanding what was
the biology of one second before, one minute, one hour,
one million years before that gave rise to it. Back to our two major
themes from day one, we are now about to be
unbound, unfettered, by our buckets, our
categorical buckets, and instead explore
their interactions. The other being that notion
from the very first class, which is that any given
point, if we’re talking about chronic
hormonal effects on this behavior, what
we’re talking about is the way those hormone
patterns were shaped during this period,
the way genes contributed to the
enzymes that make the hormones, the receptors. The second you’re talking
about genetics, all of this is becoming apparent. At every one of these
points, whatever point we are talking
about is going to be the end product of
everything to the left and just as temporary sort
of footing before going to the things on the right. So this will be our
strategy forever after now. So we start off doing
this with looking at sexual behavior,
the neurobiology, the endocrinology, the early
experiences, et cetera, et cetera. So to inaugurate the second
half of the course and the fact that it’s starting off with
lectures on sexual behavior, it has to start off with the
stupid obligatory sex joke. OK. So the Martians come to
Earth, and they turn out to be great guys. They are really terrific. They get along wonderfully
with Earthlings. All of them like
each other a lot. They’re all becoming
great friends. They pass their hours learning
about each other’s planets. What’s the weather like there? What are sports like here? What are recipes? Everybody’s getting
along terrifically. And eventually, the
Earthlings and the Martians are getting along well
enough that they get around to asking the question that
everybody is really interested in, which is, well, how do you
folks go about reproducing? So the decision was made. The Martians are
going to go first. So they clear out a big space,
and a whole bunch of Martians come in there and they stand
on top of each other heads, and their noses flash
different colors, and steam comes out
of various orifices, and there’s clanking
noises and whatever. And out pops a new
little Martian. And the Earthlings say,
wow, that was great. Love the concept. And I got great video of that. And that’s terrific
and all of that. OK So that’s worked out. And now it’s the humans turn. So a willing couple is found,
and some space is cleared out. And the Martians sit down
there with their video cameras as well. And clicking away. And this couple goes at it. And they finish the whole thing
in a sweaty mess at the end. And the Martian say,
that’s wonderful. That’s so interesting. You Earthlings are just endless. And the fascinating
things you do, but we have one question
though, which is, so where’s the new human? And they said, oh,
that takes nine months. They say, well, why were they
in such a rush at the end? So our first question
here is, why were they in such a rush at the end? OK. Three possible answers. Choice number
one– vote for it– why were they in such
a rush at the end? Number one, because they
were acting with this fervent desire to do something for
the good of the species. Just seeing if any hands go up. That’s a good thing. Option number two,
doing that because you want to maximize the number
of copies of your genes passed on to the
next generation. Option number three,
because it feels good. OK. One hand goes up. And I’m not sure what that
indicates about everyone, but I will remind you from
the survey in the first class there that a far greater
percentage of you want to learn about depression
than about sexual behavior. So there you have it with
the Stanford experience. OK. Because it feels good. And what we deal with
here right off the start is this important dichotomy
between proximal and distal explanations for behavior. Explanation, a
distal explanation, for sexual behavior,
parentheses, why were they in such
a rush at the end? Passing on copies of
your genes, the effects of hormones, and
certain reward pathways in the brain, all of that. Proximal mechanism being
that it feels good. And starting off right
off the bat the thing to make sense of
with sexual behavior is it is driven by this
amazing little loop here of sensory stimuli,
and feedback, and immediate sensations that
drive the behavior coming out. And all this stuff down here
is for the doctoral thesis somewhere down the line. That’s not what
the motivation is. Probably more than any other of
the behaviors we will look at, the driving forces are
very proximal ones. Nobody sits there and figures
out how many copies of genes they are passing on and thus are
willing to speed up to produce a new human nine months later. It is instead, in
species after species, it is proximal
motivating mechanisms for generating the behaviors. OK. So beginning to look at
the actual behaviors, there is a funny duality to
making sense of sexual behavior across different species,
a funny sort of contrast. The first one being that, well,
all species go about sex– or all vertebrate
species go about sex in a roughly similar way. Yet, you don’t want to be
too similar to the species next door. There’s an interesting
sort of dichotomy there. All sorts of vertebrate
species are doing things with pelvic thrusting
and orgasms and– hey, stay tuned that’s
coming– and ejaculation, and lordotic reflexes,
and things of that sort. Highly conserved fixed action
patterns across lots and lots of different species. None the less, amid that,
you’ve got this other problem, which is you want to have these
fixed action patterns being specific to your species. You do not want to mess up. So there is this
strange simultaneity of very, very conserved
basic building blocks of the fixed action
patterns of sexual behavior. But along with that, a lot of
selectivity within species. Now how does that
selectivity begin to work? What you get is this very
interesting interplay, this intercalation, between the
releasing stimuli and the fixed action pattern. What you get is this
chaining of behavior. In other words, the fixed
action pattern of one of the individuals constitutes
the releasing stimulus for the other individual’s
fixed action pattern, which constitutes the releasing
stimulus for this individual’s fixed action pattern. This chaining of
transitions there, of interplay between
these two, which is where you get the
species specificity from. OK. So in terms of making
sense of that, of course, any of this in terms of looking
at the general features of how to think about sexual behavior
across species, of course, what you have to have out the wazoo
is your basic ethology credo of interviewing an animal
in its own language about its sexual
behavior, wonderfully summarized in this quote by
Martha McClintock, researcher. I think I’ve used
this quote already, which is, in her
particular case, studying female rat sexual
behavior, which turns out to be this very ornate
process involving a lot of running around
on the part of the female. Studying female rat
sexual behavior in a cage is like trying to study swimming
behavior of a dolphin in a bath tub. You need to get it in
the natural setting, or else you are going to
lose all sorts of insight. In the particular realm of
female rat sexual behavior, the standard picture
for decades and decades, the centuries where our
finest minds have looked at rats having sex,
the standard dogma has been that the female role
is a very passive receptive one. And it turns out it’s a
very passive receptive one if she doesn’t
have enough room to run around and do all sorts
of courting stuff on her own, all sorts of proceptive sexual
behaviors, which she can’t see, if you’re studying an animal
in a setting where they can’t speak in their own language. So a big, big vote for
ethological logical principles when it comes to this. All right. So just to get some jargon
under our belt right from the start here, in terms
of how the professionals talk about sex when they’re
talking about sex and trying to sound
like professionals, here are some of the terms. Old outdated term,
Freudian term, that nonetheless has
entered the general world of referring to sexual arousal
and motivation– libido. Libido, as we will see that
commonplace everyday usage term, is perhaps more
technically described as horniness. But it can also be
described as one term within a trio of the terms
that people in the business really use most frequently–
attractivity, proceptivity, and receptivity. Quick, get to work on poems
about those three terms. But what you’ve got
here is attractivity, how attractive an individual
is to someone else. Receptivity, how
receptive that individual is to the interest of
the other individual. Proceptivity, the
active behaviors that are carried out in
response to being attracted to. And thus, you could say
because of the attractiveness of this organism,
this other organism began proceptive behaviors
which did or did not prove to meet with receptive
fixed action patterns and responses. The very words any
of us would use to describe what
goes on at a party. OK. So we’ve got that triad
there, the terms that are much more in common than
terms like libido or arousal or motivation. These are the more common ones. What is another realm, in
terms that are much more used, these are much
more zoology terms. What’s used far more
often in clinical medicine is a description, a
dichotomy, between motivation and performance. And that is never used more
frequently than in the realm of making sense of
sexual motivation in men as dissociable
from erectile function versus dysfunction,
motivation being very, very different from performance. So that’s another
realm of distinctions. Other realms as well–
desire, orgasms, arousal, all sorts of commonplace terms. The performance versus
motivation dichotomy and the proceptivity,
receptivity, [INAUDIBLE] are the major terms
that are used. Next issue, in terms
of getting to this, how do people find
out information about sexual behavior? One option is to sit there
with night viewing goggles. And that’s very useful
for nocturnal species. But how do people find out
about human sexual behavior? All sorts of ways
over the years, starting with anonymous
questionnaires. But a really clever technique
was worked out in the 1980s. A biological mathematician
named Joel Cohen getting at how to get
people to tell you about very embarrassing things
about their sexual lives. And this was prompted in the
80s when AIDS first swept in, and it was wildly,
wildly taboo at the time in virtually every
corner of this country to admit to having a less
than standard, white bread sexual orientation. Take a look at the extended
notes to see the trick that Joel Cohen came up
with, a very clever device in order to figure out
what percentage of people are doing what sexually
without asking anybody to give an answer that
they would find, perhaps, to be embarrassing or grounds
for all sorts of persecution. OK. So beginning to look at
aspects of behavior and other features of the rightmost
end of all of this. We start off with the
most central puzzle in making sense of any of
this stuff, which is, so what’s up with female orgasms? And we’ve got right off
the bat the simple problem of making sense of this
biological phenomenon and one where fertility is
not dependent on it. One does not need to have
orgasms to become pregnant, to give birth, to pass
on copies of one’s genes. So what’s the deal with orgasms? First off, a question
we will wind up asking with a whole lot of the
behavior coming down the line is, are we the only species? And all sorts of
careful studies have shown that we are
not the only species. Other apes, other
primate species, as well monkeys and apes, show
orgasm among the females. And that is detectable by
all sorts of physiology we’ll hear about in a while. We are not the only species. One of the really
bizarre, pathetic things about trying to do
research in this area was one of the first papers
that ever demonstrated something which physiologically was
identical to female orgasm in rhesus monkey
females, which wound up being a paper in
this journal Science. Down there in the
footnotes, the authors had to indicate this did not
make use of any federal grant money to carry out the study. Just to give you a sense of
where some of the stuff sits. OK. So what’s up with female orgasm? It is not necessary
for conception. It is not necessary to
increase the number of copies of your genes in
future generations. Despite that, there
is some evidence that it facilitates
fertilization. And the technical term that’s
always been given for that is, bizarrely
enough, facilitation. The notion is something about
the vaginal fluid, something about the biochemistry of,
increases sperm motility. Sperm swim faster and harder
and jump upstream back to spawn or whatever it is
the sperm are doing with more avidity, with
more energetic displays, in an environment of
more vaginal secretion. And orgasm greatly
increases that. So the argument there
being that orgasm facilitates fertilization
through the sperm facilitation process. Evidence for that has always
been a little bit indirect. It is not airtight
that that happens. Another argument for why
this increases fertility. And this is sort of
an interesting one. And the notion here is that
what an orgasm does is, among other things,
exhausts you enormously, causing you to be
far more likely to be horizontal than vertical
shortly thereafter, and thus, facilitating fertilization
because the sperm don’t have to swim straight
up against gravity. I kid you not. This is one of the
leading models out there. Then there’s the orgasm
facilitates female conception out of reinforcement
theory, which is back to the it feels good and thus
you are more likely to do it again and increasing the
likelihood of passing on copies of your genes. All of this is wonderful. All of these possible
mechanisms where, even though female orgasm is
not necessary for conception, it nonetheless increases
the likelihood of. That’s great. However, what most of
the studies have shown, though, is there
is no relationship between the fertility of
a woman and her propensity towards orgasm. It does not seem to play
out in so far as any of this facilitation
or horizontal swim enhancement techniques
or whatever actually occurs– these are not big enough
of effects to actually make a difference in terms
of reproductive success. So what else? What else is known about it? There is a certain
degree of heritability, of propensity towards
orgasm in females. And this is shown with
all our standard behavior genetics techniques in
terms of comparing dizygotic versus monozygotic twins. We know what to do in terms
of not overvaluing findings like those. Nonetheless, they are there. So if a basic puzzle is,
why do females have orgasms if it’s not necessary for
conception and, in fact, the evidence is not great
that it even facilitates it, why on top of all of
that, why such things as clitoral orgasms, which
the studies generally show are more easily
brought about than are vaginal ones,
what’s up with that? Even more the same question. Now somewhere in
there is a lurking the heart breaking
possibility in making sense of why female orgasm
exists the dreadful possibility that what we’re dealing
with here is a spandrel. And that it is a spandrel. It is simply baggage
brought along that those guys have to go
through this orgasm physiology to do any stuff with sperm
and pass on copies of genes and all of that. And it’s simply baggage
that the same physiology occurs in females. That orgasm is simply
a spandrel in women. And the counter scenario
that’s always given is, this is exactly
equivalent to the notion that nipples are
spandrels in men, in that women, female
mammals, need to go about all this lactation business. And that’s part of the
whole package deal. And just as it would be way
too much work to evolve females without orgasms,
it would be way too much to get rid of those
useless nipples on men. OK. Let’s have a quick survey. Yes? So could a lot of
those questions also be applied to why
do male have orgasms? Because ejaculation can
occur without orgasm. OK. So why do males have orgasms? Ejaculation can occur–
it is far more voluminous in the face of an orgasm. So that’s easily framed in
terms of an adaptive mechanism. OK. Quick survey here. How many people–
OK, how many guys who have those useless
nipples, how many of you go for the nipple as
spandrel in guys theory? Whoa. Is that slow in the hands? OK. Should I raise my hand? Should I not raise my hand? OK. Women in the room, how many
go for the female orgasm is merely spandrel theory? If I recall, there was one other
question somewhere a few weeks back that only got one
person fessing up to it, and it came somewhere
around there also. So I don’t know if
that’s the lighting or if people tend to
sit in the same places. OK. So not a whole lot of enthusiasm
for the spandrel concepts here. Nonetheless, that needs to
be seriously entertained. OK. So now looking at other features
of the fixed action patterns, and amid all these
different species doing lordotic stuff and
orgasms and ejaculation and all of that, what are some of
the realms of sexual behavior that are relatively
unique to humans? First off, one that used to be
thought to be absolutely unique was non-reproductive sex. This is a world of difference
than those species where the female ovulates for like
2 and 1/2 hours every year, and everybody mates
at that point. Or species where
somebody comes into heat, a female is in estrus. Humans have
non-reproductive sex. And that was viewed
as absolutely unique. What it is now clear is it
is not completely unique. There are lots of
other species that do, probably most famously bonobo
chimps and various cetaceans like dolphins. Nonetheless, it is certainly
a specialty among humans. What else? Foreplay, that used to be in the
category of human specialties. And it is clear by now that
bonobo chimps, for example, have vastly more
patience with foreplay than average humans do. We are not the only
species with that either. Huge, huge controversy. How unique is homosexuality
to human behavior? Human sexual behavior? And what’s clear increasingly
is we’re not the only species with that either. The original view, when people
would view homosexual behavior, male-male, female-female,
in other species, it would be animals
in captivity. And it would be
the, why is there so much homosexuality
in prisons argument– lack of alternatives. This was not normal,
natural behavior. What is clear from
ethological field studies is we are by no means
the only species to have homosexual behavior. What else? One of the things that we do
seem to be fairly unique about is having egalitarian
sex, which is to say that there are
no human cultures where as part of the central
tenets of that culture people are restricted, only a
subset of individuals are allowed to reproduce. And this is a
world of difference from various species. For example, New World
monkeys, marmosets, where it is only one
male and one female in a group that does
the reproducing. Instead, humans in every culture
ever seen have egalitarian sex. What else? What else is highly human? People used to
think exclusively so this endless quest for variety. And again, just take a look
at these bonobo chimps, and you’ll see how small minded
we are when it comes to this. But something else
that is indeed unique to human sexual
behavior is the notion that this is something
you do in private. There is no other species where
the majority of sexual behavior is conducted intentionally
outside the sight of everybody else. That is rather unique to humans. What else about
human sexual behavior seems to be specializations? One that is fairly unique,
if not entirely so, is the subset of humans who
psychopathological confuse sexual behavior with violence. And that seems not to have
a whole lot of precedence. So immediately one
asks other domains. Masturbation, that is not
remotely a human specialty. That has all sorts of
other species as well. And that used to get the,
well, what else is there to do when you’re sitting in
the zoo– for the animals– what else is there to do? It is not natural. It is a default whatever. But looking out
in the real world, and there is plenty of that. And one of the most like
implausible suggestions for an adaptive
just so story thing is, why do male
primates masturbate to the point of ejaculation? They tend to eat
the semen afterward. Whoa! Great source of protein,
go the adaptationists. Everything has an
adaptive basis. This one does not ring
terribly true to me. What else? Fantasy. Fantasy in humans, is
that unique to humans? Obviously, we haven’t a clue. But here’s one suggestion to
me that this is not actually the case. And this was years ago where
I was watching my baboons, and there was this
one low ranking kid, this snivelly adolescent kid,
where the nearest thing he has ever gotten to a
female in his life with some high ranking female
in a bad mood beating on him. And he’s sitting there
minding his own business. And along comes, I think by
any baboon male standards, the hottest female in the troop,
who has a peek estrus swelling, is no doubt ovulating that day. Comes walking along,
followed two feet behind by the huge
menacing male, who was in the
consortship with her. And our guy just sits there
and doesn’t even quite look at what’s happening. Every now and then, his eyes
go up, watching them go past. And as she walks past,
he gets an erection and then goes off
and masturbates. OK. The charming– I don’t
know if this is even the word you can use
in this setting– but the charming notion is
that we’ve just seen evidence for some sort of internal
fantasy life going on this guy. OK. You could be a killjoy
instead and say, no, no. She was giving off
wafts of pheromones, and that was what was
responsible for it. Nonetheless this is
about as far as we can get at asking this
critical question, are we the only species that
does this fantasizing stuff? Marriage. Clearly, we’ve heard about
monogamous pair bonding species. In terms of the formal structure
of marriage, it is universal. All human cultures have
some version of it. Across all human cultures,
more than 90% of people wind up in that
culture’s equivalent of a permanent,
stable relationship. And this is the case
in polygamous cultures. We’ve already heard
that business. Even though historically, the
majority of human cultures have been polygamous,
nonetheless, amid them, the vast majority of
individuals have been in monogamous relationships. Amid that, nonetheless,
what is also clear is amid that highly,
highly prevalent pattern of monogamous relationships,
there’s a lot less monogamy going around than
you would think. And this was first sorted
out– people like Alfred Kinsey when first working out
that questionnaire approach to people’s sexual
behavior, what became clear was there is a lot less
faith within pair bonding, within humans in this
country and has since shown in all sorts
of other societies than one would
originally assume. There is social monogamy but
not necessarily anywhere near as high of rates
of sexual monogamy. And what the paternity
studies have shown is in most Western
European countries, the rate at which children
have been fathered by an individual other
than the person claiming marriageable credit for doing
so ranges between 10% and 40% of children. How’s that for a number? OK. What else? What else tends to be a feature
of human sexual behavior? What you have is, of course,
not only intrinsic in the fact that there’s a difference
between social and sexual monogamy. You have cheating. That is a human specialty
in every culture. What else is absolutely
wildly human? This notion of romance. And romance is,
by most estimates, a relatively new invention
in most cultures, maybe a couple of centuries old. And what is an even
newer invention is the notion that romance,
passion, et cetera, should persist, should last
throughout the entire duration of the lifetime’s marriage. That is an utterly
novel concept. That is perhaps 30,
40, 50 years old in most Westernized countries. That’s a new one as well. What that, of
course, ushers in is looking at issues of divorce. Across all cultures, the
average duration of marriages are two to four years. And people have
made the argument that that is the typical
duration of children being dependent on a high
degree of parenting, of both parents being around. That is the average interbirth
interval, two to four years, in most traditional
human cultures. What’s the term
being described then if that is the “natural”
point at which most marriages dissolve and turn into
other monogamous relationships? The term that is
given is that humans tend toward being serial
monogamists, moving from one monogamous relationship to
another with, on the average, a lag time roughly corresponding
to the interbirth interval. So that’s charming. What else? What else do you have? All sorts of other aspects
of human sexual variety, but ultimately, when you
look at human sexual behavior versus other species,
we are so boring. We are so limited when you look
at the range of unlikely things going on out there. Species that are
regularly hermaphroditic– and people, in fact,
have done studies on how is it that a
hermaphroditic animal does not try to have sex with itself? And these are usually
worm type things. And that’s some version
of an incest avoidance. At the same time, there are
other species where individuals change sex opportunistically. All sorts of fish species
where that happens. Lots of species that
are parthenogenetic, where an individual reproduces
without the benefit of anybody else’s genetic input. Even stranger, there’s a bunch
of snake species that are parthenogenic, but the
females cannot reproduce parthenogenically unless
they mate with males. They do not actually get
any sperm from the males, and they get no
genetic contribution, but something about
that is necessary for the parthenogenetic
event to occur. OK. So all sorts of bizarrities that
make our fixed action patterns look really pretty dull. But nonetheless, these are the
backbones of the human fixed action patterns,
and some of them wildly unique, some
of them far less than people used to
think, some of them very, very unprecedented. OK. So what this allows us to do
now is make our first big step. What’s going on in the brain? What is the neurobiology
of sexual behavior producing those fixed
action patterns? And what you better bet
right off the bat is we are talking about
the limbic system. This is all limbic
system until we see ways in which it’s not
just all the limbic system. But it is heavily
centered– no surprise– in the limbic system. And this was being noted
first around the 1930s, 1940s with the first experiments where
there were lesion studies done damaging different parts of
the limbic system in animals. And what would be noted
was animal sexual behavior would change. And this was eventually
termed a profile, termed after the two scientists
who pioneered this stuff called the Kluvre-Bucy Syndrome,
which is when you damage some of these strange mysterious
rhinencephalonic structures in there, you change
the sexual behavior. You change, for
example, in monkeys, whether they are attempting
to mate with another monkey as opposed to an inanimate object. They change aspects of
the fixed action patterns of the behavior and such. And out of it, this was
one of the main driving forces on people saying,
nose-brain, well, that’s great. But actually, what
we’re looking at is a part of the brain that
has lots to do with emotion and emotionally
related behaviors. That was one of
the driving forces on the limbic system being
pulled together as a concept. OK. So what areas within the
limbic system are relevant? First pass, there are
different hot spots in there depending on gender. Among females, probably
the most important area is a subsection of the
hypothalamus called the ventral medial
hypothalamus involved in female sexual behavior. What’s the evidence for that? Just go back to last
Friday’s lecture– lesion studies, stimulation
studies, recording studies. Destroy the VMH, you do not
get sexual behavior anymore from a female. Stimulate it, and you will
get the same behaviors that you would normally
only see in an ovulating female rat for example. All the sorts of
tools we heard about. Reinforcing this
even more is this is the hot spot in the
hypothalamus for receptors for estrogen and progesterone. So that makes lots of sense. Meanwhile, another region of
the brain that is typically involved in sexual
behavior in females, a region in the midbrain. The midbrain, which seems to
have something to do with some of the hormonal aspects
of sexual behavior that are specific to females. Finally, back to
that lordosis reflex, you got to have a
spinal cord to pull off the full array of typical
mammalian female sexual behavior. So spinal pathways,
which do not exist in males, lordotic reflexes,
the back arching reflex, is exclusively a female one. Meanwhile, over on the
other side of things, there are regions
in the brain that tend to be more specialized
for sexual behavior in males than in females– a different
part of the hypothalamus called the medial preoptic area. And the exact same
sort of evidence is for the ventral
medial hypothalamus in females– lesion studies,
stimulation, recording studies, all that sort of
thing, and– you guessed it– whopping
great amounts of testosterone receptors,
androgen receptors, within the medial preoptic area. Very interestingly, something we
will hear more about next week or so, is another
region of the brain is involved in male
sexual behavior, which is the amygdala. Mhm. That’s kind of interesting. The amygdala. We’ve already heard about
amygdala fear, anxiety, and all of that. But the amygdala also plays a
very major role in aggression. And there’s a little
bit, a small domain, of amygdaloid function
in males that’s involved in sexual behavior,
involved in sexual motivation. Medial preoptic area is much
more about sexual performance in males. Amygdala is much more
about sexual motivation. And all sorts of people have
speculated fairly reasonably, I think, that this
may have something to do with the fact explaining
why, among humans, it is far more likely to
be males than females who go about confusing
sexuality with aggression. That it’s got something
to do with this weird role of the amygdala in
male sexual motivation, male sexual arousal. What else? OK. Males have penises, thus
they’re the only ones who can have penile
erections, and to do that, autonomic nervous system. And what we will hear
about, what you already heard about in the introduction
to the autonomic nervous system, but also in
the zebra’s book is that whole business in order to
manage that, to pull that off initially, it is
parasympathetic nervous system that establishes the erection. The process of arousal involves
the transition to sympathetic. Full blast sympathetic
nervous system needed for ejaculation, that’s
what all of that is about. Exclusive to males. But then it turns out it’s
not exclusive to males because it’s virtually the
exact same physiology underlying clitoral erections in females,
the same exact sort of thing, which, of course, brings up
the dangerous possibility of another spandrel in
our laps here in terms of making sense of that. I didn’t say that just now. Did I say spandrels in your lap? OK. Bringing up that
possibility that is not specific to male physiology. What is specific,
of course, is stuff that’s going on with penises
in terms of blood flow. There’s generally a
dichotomy between species, between whether or not
males get vascular erections or muscular erections. Vascular erections, you increase
blood flow into the penis, and you stop it from
going out the other end. And thus, you get a
vascular-driven engorgement as DH Lawrence would no
doubt have described it. Alternatively, in
lots of species there are muscular erections. There is a muscle, for example,
found in rodent penises called the erector [? levae ?]
muscle– well, that’s not too surprising
that it’s called that– and a whole bunch of
cell bodied neurons in the spinal cord responsible
for pulling up the sail or whatever it is you do there. And what you get are
differences in general. The muscular-driven
erections occur a lot faster. The vascular ones,
the hemodynamic ones, last a lot longer. Take your pick, but
it’s essentially the exact same autonomic
physiology in both cases. Finally, one other
thing, a factoid, a useful one we heard last
week, which is insofar as there is very
similar physiology to orgasms in both sexes,
there is that difference in recovery time,
how long it takes for the sympathetic
nervous system to go back to
baseline post orgasm. And on the average,
a substantial sex difference in that. Yes, everybody managed
to guess it last week, which direction it went. A far slower recovery time
in females than in males. In terms of underlying
neurobiology, something that was a
major finding in the field were brain regions that
differed in size depending on your gender,
including in humans. And this ushered in a whole
world of sexual dimorphism in the brain. And there have now been shown
to be all sorts of brain regions where, on the average,
you get differences in the size of nuclei. You get differences
in the number of axons going through a
bundle of fiber, all of that. And we will hear about some
more of those down the line. But the one that has gotten
the most attention in terms of sexual behavior is a
cluster of tiny nuclei in the hypothalamus
called the INAH cluster, the Interstitial Nucleus of
the Anterior Hypothalamus. Do not write down
what that stands for. But it’s a little
nucleus in there there, a little subset
of neuronal cell bodies, where you get a very
substantial sex difference in the size of this area,
where on the average, it is about twice the
size in men as in women. And back to the
other week’s rant about statistical
significance versus magnitude, this is a big effect. It is almost,
almost in the range where you can identify
the sex of somebody by looking at the size of
this nucleus in their brain post-mortem. In rodents, you pretty much can. A very reliable two-fold
difference, males larger than females. As we’ll hear in a while,
one really interesting exception to that. OK. So either some areas of the
brain that are preferentially involved and activated
by sexual behavior, depending on your gender,
or regions that differ in size substantially
by your gender. But then, at the end
of the day, there’s all sorts of things that
are absolutely in common. Again, the physiology of
orgasm, exactly the same. What clinically the
picture is is males having problems with the whole system. The problem tends to be
too rapid of a transition from parasympathetic
to sympathetic. In other words, the world
of premature ejaculation. The more typical
medical problem in women is failure of the
transition from parasympathetic to sympathetic,
inability to reach orgasm. And it is, of course, a huge
social, cultural, political, philosophical
argument whether that counts as a pathology or
normal human variability. I’m not going anywhere
near that one. But nonetheless, that is
the more common pattern. Neurobiology that’s
absolutely in common between the sexes, which
is all of that stuff at the very beginning of why
are they in such a rush at end, the neurobiology of pleasure,
and the neurobiology of reward, and of anticipation. And this is this
whole world of– as we know already– dopamine. The role of dopamine
in sexual behavior is virtually identical
in both sexes, which is to say it plays a huge role. You find circumstances
where you deplete dopamine from the relevant
brain regions– back to last Friday–
limbic system. You remember that
ventral tegmental area, which sends that big
dopaminergic projection to the nucleus accumbens,
which then passes it on to all sorts of
places in the brain. Deplete that
pathway of dopamine, and you’re not going to
get a whole lot of interest in sexual behavior. You’re not going to get a whole
lot of libido proceptivity. What’s the classic
circumstance where you see depletion
of dopamine there and loss of proceptive libido? Clinical depression. That’s one of the defining
symptoms of depression amid the various numerous
forms of pleasure that go down the tubes. Loss of sexual interest, one
of the defining symptoms. So the dopamine system. The general term
given for that is the mesolimbic dopamine
system to distinguish it from some of the other ways that
dopamine is used in the brain. The mesolimbic
dopamine system is absolutely central to
the reinforcing aspects of sexual behavior. So what’s the evidence for that? First off, back to
that distinction that I think I brought up
last week– I wasn’t paying attention– but I
think I talked about, which is the dopamine
system there is not so much about reward, it’s about
the anticipation of reward. Did I talk about that in
monkeys pressing levers? Yes. OK. I should probably read the
extended notes at some point or look at the film of this. OK. What you see there
is the dopamine is about the anticipation of. And the dopamine,
as we heard, is about also fueling the behaviors
needed to achieve the reward. Dopamine in this
mesolimbic pathway as driving
goal-directed behavior. And that is certainly the
case with sexual behavior. By now, there is a whole
literature involving humans where you stick them
in brain scanners and you do something
or other sexually arousing or interesting or
something or other to them. And then you see what parts
of the brain activate. And it’s these dopamine pathways
consistently way up there. Showing just how subtle
this can be, how’s this? You take men– there’s been a
whole literature by now showing that you present people in
brain scanners with pornography. And that must have been a really
interesting in human subjects release form you worked out. But showing in both sexes,
what you tend to see is activation of
dopaminergic regions. We will hear in a little
while a sex difference in that domain that will
probably not surprise anyone. But how’s this for subtle? You take a guy, and you
show him the picture of someone of the opposite
sex if he is heterosexual. And you show him the
picture of this individual. And if it is someone who he
assesses as being attractive, you don’t necessarily get
this dopaminergic pathway to activate. It depends. What this study showed was
if the person is making what would pass for eye contact, if
they were looking straight out, the dopamine system activates. And if they’re looking
elsewhere, it doesn’t activate. How’s that for a classic
male sort of responsiveness? If it looks as if this
attractive person is looking at you, it activates. Even more distressingly
from this study, when you show men–
on the average, blah, blah–
pictures of women who they would rate as
being unattractive, it’s when they’re looking
away that the dopamine system activates. Oh my god! What is going on here? This is pitiful. What also has been shown is
the exact same eye contact phenomenon of gay men looking
at pictures of attractive men. Another theme we’re going
to see over and over, which is sexual orientation
being pretty much trivial in terms of
how it influences some of this neurobiology. Just switch the gender
of the other individual, and it works exactly the same. Now when you look at this
business about dopamine rising in anticipation of a reward
rather than a response to the reward itself, it
brings up one of the– it doesn’t bring that
up– it brings up one of the all-time
interesting studies that was published
about a decade ago. OK. So the paradigm I
described last week, you put on the light, which
tells the monkey that, OK, we’re starting
one of those sessions where if you press
the levers adequately, you will get a reward. And they now carry
out this behavior. And as a result, they
get the reward here. And as we saw, dopamine
doesn’t go up after the reward. It goes up at this point. This is the I how to do this. This is going to be great. This is terrific. Here’s where you get
the rise in dopamine. This is not only
the anticipation, but if you don’t
have this rise, you don’t get the behavior,
the goal-directed behavior. Now in this brilliant
study, what they did was transition from
a paradigm where, OK, the monkey presses the lever
10 times and gets the reward. Now what you do is
the monkey works, and it gets the reward
only half the time. It gets only a 50% reward
rate unpredictably. And what happens to dopamine? OK. Got your choice. What’s your vote? It doesn’t rise as much. It rises the exact same amount. It rises even higher. OK. You guys all understand
anticipation and goal– it does this. It’s one of the
biggest rises you will find in dopamine in
the brain short of cocaine. What have you just
introduced into there? This is, I’m all over it. I know how this works. This is going to be great. I have mastery and control. I am the captain of
my own lever pressing. This is all about that. What’s this about? This is what dopamine
does when you’ve introduced the word
maybe into the equation. And that is incredibly
reinforcing. And people will work like
mad in contexts of maybe far more so than when they
work in contexts of certainty. Psychologists have
known this forever. This is intermittent
reinforcement. You never get more
behavior out of an organism than when you have
introduced a maybe into it. And part of the
brilliance of this study was what they then did. Now animals either got
reward 25% of the time or 75% of the time. On a certain level,
these are diametrically opposite manipulations. In one, you’re
getting more rewards. In the other,
you’re getting less. What’s the thing
they have in common? They both had smaller
maybes than the 50% version. And what you see is it
would look like this. 100%, 25% or 75%, 50%
maximizing the maybe. And one of the most
brilliant things that various social
engineers do with humans is convince people that there’s
a 50% maybe when it is not 50% in the slightest. That’s what Las Vegas is about. That’s an entire world of very
smart psychologists making people think in
circumstances where there’s like one tenth of 1% of a maybe
going on there that is actually a 50%. And when you do that, you
get dopamine like crazy, and you get
goal-directed behavior as a result. Really,
really powerful. And this is so strongly the case
that this explains an extremely cynical thing that a
guy I knew in my dorm back when used to
say all the time. How’s this for like a
dispirited view of what life is like, but possibly
absolutely accurate, which is, a relationship is the price you
pay for the anticipation of it. How’s that for a grim worldview? Go figure. This guy had– what a string
of disastrous relationships. But what you see here
is introduce a maybe, and it is very, very powerful. One final piece of the dopamine
system here that is pertinent, which is, as you
might expect from all of our molecular
biology stuff, there’s all sorts of different
dopamine receptor subtypes. And two of them are pertinent
to this world of sexual behavior and reward, what is called
the shockingly the D1 dopamine receptor and the D2
dopamine receptor. And what studies show is
in monogamous species, what happens is right after mating,
when a pair bond is first formed, the second that’s over
with, levels of the D2 receptor go way down. You down regulate the
levels of the receptor, and you up regulate the
levels of the D1 receptor. What’s that about? If you drive down the D2
levels before they even mate, they don’t form a pair bond. If you prevent the decline in
the D2’s after they’ve mated and pair bonded or if you
prevent the rise in the D1’s, they’ll pair bond. And then, 8 and
1/2 minutes later, they will go and pair
bond with somebody else. The D2’s seem to mediate the
rewarding anticipatory aspects of pair bonding. The D1’s, on a certain
rodential level, seem to mediate the pleasure
of the monogamous, the truly monogamous features
of the pair bond. So a very interesting
interaction between the two. OK. One last thing about
dopamine, and this one is like even more depressing
than relationships are the price you pay. This was a study which
was really like someday may come to haunt you majorly. And in this study,
what they did– it was another one of those
brain imaging study ones. And what they did was they
took people in two categories. In both cases,
these are people who had found their beloved,
their beloved, the person who was their soul mate,
the person in whose arms they were going to die
someday, the person. And they divided it
between these two groups. One was a group where they had
known the person in whose arms they were going to die
for like 2 and 1/2 weeks. And the other is when
they had been together for more than five years. So you put somebody
in the brain scanner, and you start flashing up
at speed, subliminal speeds, of pictures of
individuals they know. Important control in the study. And embedded in there is a
picture of their beloved. And suddenly, somewhere
along the way, up flashes the picture
of their beloved. Be in a short-term relationship
and the dopamine system goes crazy and
activates like mad. Now, you come back
five years later into that same relationship
with the beloved, and you do the exact same thing. And you flash up their picture,
and the dopamine system doesn’t activate. What activates instead was
that anterior cingulate thing we heard about on Friday
having to do with empathy, and comfort, and all of that. In other words, what we see here
is the neurochemical transition from one’s beloved
from causing your blood to run scalding hot
to your beloved being like a comfortable old armchair. This is one depressing study. So let’s take a five-minute
break to contemplate that one. OK. And then we will resume. Lots of good questions
just now during the break. Disappointingly few
along the lines of, I’ve got a friend who. So not a bunch of those. But let’s see. A number of questions. First one, can I repeat what
I said about the D1 and the D2 receptors? OK. These are different types
of receptors for dopamine. In other words, they all respond
to the same neurotransmitter dopamine, but in different ways. And these receptors are found
on different neuron types. So you’re getting into all
sorts of different pathways. What you see is, in rodents,
in pair bonding rodents, they better have
elevated levels, they better have D2
receptors on neurons being fed by this mesolimbic
reward dopamine pathway. They have to have D2 receptors
to form the pair bond for the attachment to occur. The second that happens, you
need to have low levels of D2 and high levels of D1 to remain
faithful in your pair bonded relationship. So what you see in these voles
is right after the pair bond occurs, there’s down regulation
of the D2’s and up regulation of the D1’s. And if you prevent
that from happening, the pair bond that’s been
formed does not prove lasting. So that’s what I
was saying there. Somebody brought up
the great question, which I was going to say
something about and forgot, which is, well, how
about like the D2 D1 ratios in humans and their
sexual behavior stuff? And there’s been
one study showing that a higher ratio
of D2 to D1 predicts more stable relationships. Small effect. Not replicated yet. But nonetheless, that’s
kind of interesting. So on a certain
level then, D2 seems to be required, at
least shown in rodents. Who knows about us? D2 is about the formation
of the attachment. D1 is about the maintenance
of it, the faithfulness of it, if you will. Next, somebody
bringing up the issue in terms of female orgasm. Maybe what female orgasm is
about is a mate selection mechanism, as in
individuals who increase your likelihood of
having orgasms are ones you are more likely to
lower your D2 receptors for. But the one problem
with that one that makes wonderful sense–
what the studies tend to show though is the
likelihood of orgasm is much more a function
of who the female is than who the male is that they
are with, arguing against that. Let’s see. Finally– no. Not that. OK. So we already covered that. And there was one
additional question. OK. So what’s the driving
force in terms of the proximal reinforcing
pleasurable aspects of sexual behavior? What’s up with why
only some species– us predominantly– have
non-reproductive sex, can have sex all the
time, versus other species that only do for reproduction? What that means is
in other species, the endocrinology of
ovulation is the thing that makes sex pleasurable. And we will see shortly
what that’s about. In females, it’s the
hormones associated with ovulation that
sensitize various tactile receptors to respond in ways
that mediate proximal pleasure. And in males, it’s
the female giving off, for example, the right
pheromones, the right releasing stimuli, driven by the
right hormone levels that constitute the proximal signal
of pleasurable anticipation. And what you find in humans
is it doesn’t work that way. You do not need, for
example, in women the elevated levels of estrogen
typical of ovulation in order to have tactile responsiveness
to sexually arousing stimuli. Stay tuned though. It’s easier though when
estrogen levels are higher. OK. Final brain region
relevant to all of this is the frontal cortex. We already got a first pass at
the frontal cortex last week. And frontal cortex regulating
your behavior, impulse control, all that sort of thing,
gratification postponement– this plays a large role
in sexual behavior. What’s the easy
immediate explanation that one can come up with,
what the frontal cortex does is it makes you be appropriate
in your sexual behavior. It teaches you the
appropriate context. It teaches you what aspects
of proceptive sexual behavior is not a good idea. It keeps you from doing
things you would regret vastly afterward. That’s a very easy
version of it. And commensurate
with that, you see lots of circumstances
of individuals with frontal cortical damage
doing highly inappropriate sexual behavior. One example of it, and one
of those horrifying things that can happen–
this was a case that actually happened in
a nursing home in Martinez in the East Bay a
number of years ago. This was a man in his 80s
who had had stroke damage to his frontal
cortex, who was found to have raped a woman
there, another 80-year-old with Alzheimer’s disease. Damage the frontal
cortex, and all sorts of the, “this is not sexual
behavior that you do” constraints go down the tubes. Just as importantly though,
what the frontal cortex, with all of it’s giving
you the discipline to do the right thing,
some of the time, what that takes the
form of is getting you to do proceptive
sexual behavior. For example, you
are trying to do some courtship of some
other antlered ungulate that you are courting. And this is terrifying because
there is another individual challenging you. And there’s the
frontal cortex that is getting you to carry
out those sexual behaviors to that point, even if it is
a terrifying circumstance. Nonetheless, what the frontal
cortex mostly is about is reigning in sexual behavior. It’s not changing the fixed
action patterns of sex. It’s changing the context
in which the fixed action patterns occur. So now, we are ready
to look at one more feature of the
neurobiology, which is when somebody is having sex,
what hormonal responses are triggered? Notice this is not here. This is not what hormones
have to do with bringing about sexual behavior. This is, what are the hormonal
responses to sexual behavior? Starting off in females,
including human females, having sex increases
secretion of progesterone-derived hormones. And that has something to do
with reinforcing the pleasure. Interestingly, in females
the world over, having sex increases the level of
testosterone-related hormones in the bloodstream, androgens. Women, females, generate
androgens maybe 5% the levels you see in males. And they come out of
the adrenal glands. And they seem to play
a very central role in mediating sexual motivation,
sexual arousal, in females. How is that’s shown? Obvious experimental
studies with lab rats. How is that’s shown in humans? When women have any of a number
of types of diseases where you have to take out
the adrenal glands, sexual motivation, sexual
arousal, goes down. Give them replacement
androgens, and sexual arousal, sexual
proceptivity, returns, so androgens there playing a role. But probably most
importantly, in terms of hormones triggered by
sexual behavior in females, is the release of oxytocin. Oxytocin is really interesting. We’ve heard about
oxytocin twice already. One, is when it’s coming out
of the posterior pituitary. And the second is that minor
business the other day, last Wednesday,
of oxytocin being another one of those
hypothalamic hormones that helps to release ACTH
from the pituitary. Remember, it doesn’t
directly release. It’s a modulator, a CRH action,
if-then clause, et cetera. But those are the two ways
we’ve heard about oxytocin. Oxytocin also works in the
brain as a neurotransmitter and neuromodulator. And what does it do there? It appears to play
a very central role in forming attachments,
a very central role in forming of pair bonds. And it, along with dopamine
and the D2 receptors, are critical for female
voles of monogamous species to form pair bonds. Female humans, when having
sex, secrete lots of oxytocin and activate oxytocin
pathways in the brain. And it appears to play a role
in the formation of attachment. Interestingly– how’s this–
a whole body of research now showing that if
you introduce oxytocin into the brains of
humans experimentally, they become more trusting. Amazing body of research where
you take aerosolized oxytocin and you spritz it
up people’s noses. And what they showed
in the studies were, number one,
one type of study. You then play a clip of
somebody making an argument for some stance in
some debate, and people believe the person more. They find their argument
more convincing. They trust the person more. Or the other version
that’s been shown is you spritz oxytocin
up the noses of people, and you make them more
cooperative in their game theory play, the
ways in which they go about playing prisoner’s
dilemma and other games we will hear about
later on as well. This has given rise to a whole
new field– I kid you not– called neuromarketing. The notion that if only you
could spritz oxytocin up the noses of people right before
your television ad comes on, they’re going to believe
you when you say it will make you happy
to buy our thing. And they will fall for it. There are actually
neuroendocrinologists making a living now selling
their wares to neuromarketing people– self-proclaimed ones. No doubt they are
spritzing oxytocin up the noses of those
capitalists to get them to hire them to do this. But oxytocin playing
a role in this. So that’s kind of interesting. Because what’s oxytocin
mostly doing in the body? The vast majority
of oxytocin is not this stuff up in the
brain in these pathways, some of them impinging on
dopamine-releasing neurons. The vast majority is not
the oxytocin sitting there in the hypothalamus doing
something or other to ACTH in the pituitary. The vast majority is this stuff
coming out of the posterior pituitary. And what does oxytocin
have to do there? It has to do with milk letdown. It has to do with nursing. And suddenly, instead,
it’s playing a role in forming sexual pair bonding. And the argument is
made that attachment, monogamous attachment, sexual
attachment, is in some way, evolutionarily a descendent
of the neurobiology of mother-offspring attachment. That that’s where it is
originally being driven by. So oxytocin playing
a role there as well. Meanwhile, over at the
male end of things, up go testosterone
levels during sex. In a surprisingly linear
way, the more sexual behavior in a male, the higher
testosterone levels are found afterward. Critically, critically–
stay tuned for a little while– these are elevations
of testosterone in response to sexual behavior. As we’ll see, the evidence
that high testosterone levels make males more sexually active
is basically nonexistent. So critical, critical
proviso here. This is sex increasing
testosterone secretion, not the other way around. What else? Meanwhile, back to the
posterior pituitary. Was that a question? No. OK. That was a head scratch. OK. Back to the posterior pituitary. The other hormone coming
out from there, vasopressin. And oxytocin is to females
as vasopressin is to males. And we’ve already
heard something about this back in
the molecular genetics stuff in those if-then clauses
and unlikely ways in which you get mutations. vasopressin, vasopressin
also is found in the nervous system, where it
serves as neuromodulatory role. And vasopressin is critical
for forming a pair bond. Back to that business
about when you look at monogamous versus
polygamist species, what’s going on? What you have uniquely
in the monogamous species is expression of
the vasopressin receptor gene on neurons that
released dopamine. In other words, male
secrete vasopressin. And if you are of a species
where vasopressin now goes and stimulates dopamine
neurons, you decide you really, really, really liked having
sex with this other vole. And you come back for more. And that’s the driving force on
the formation of the pair bond. Incredible studies
showing that if you take male voles from
the polygamist species and, due to gene
transfer techniques– I’ve mentioned the
study already– but you now stick
vasopressin receptors into those dopamine neurons,
those polygamist males now become pair bonding males. They now become monogamous. So really interesting. What you then see
in these studies is you look at these monogamous
species where the males have vasopressin receptors on
these dopamine neurons, and you look at
individual males, and the ones who
have more receptors there are forming
pair bonds faster. It takes fewer rounds
of mating with a female to form a pair bond. So what about primates? So you start off looking at two
different primate species, one pair bonding, marmoset monkeys,
New World marmoset monkeys, and then one classic
tournament species, polygamous primate
species, rhesus monkeys. And what you see is
you’ve got the variant, the monogamous vole,
vasopressin receptor gene variant in the pair
bonding monkey species, in the marmosets. And you get the
polygamous version of the gene in the
rhesus monkeys. So it maps on there as well. So the more of this receptor
in these dopamine pathways within monogamous
species, the more rapidly they form a pair bond. And what you see is differences
in the mere presence of them in comparing pair bonding
versus non-pair bonding rodents and monkeys. So how about humans? First thing that comes
up is, among the apes, you also find the two
variants, the monogamous vole variant of the
vasopressin receptor gene and the polygamous male variant. So what species
do you see it in? In chimpanzees, you see
the polygamous vole species version. That makes lots of sense. They are a major polygamist
species in their behavior. But then, this
beautiful dichotomy comes crashing down
when you see that you’ve got the monogamous gene
version in bonobos. And as we will hear
about in a while, bonobos are the most
hyperpolygamously, hyper varietyish sexually behaving
organisms on the entire planet. They are as far as you could
get from a monogamous species as you can ever ask for,
if you ask for such things. And you’ve got the wrong type
of vasopressin receptor gene. Whatever is going on,
it’s more complicated than the have the
version that winds up on the dopamine
neurons and you are going to have 50th wedding
anniversaries if you are a vole or you are a marmoset. And it’s got to be more
complicated than that. So how about humans? And what you see
is not explicitly as much genetic
variability as some people having the monogamous vole
version and some people have the polygamist. But nonetheless,
you get variation. The gene basically is
about halfway in between. Whoa. We keep having that
theme over and over, all these different ways
of looking at body size, and sexual dimorphism,
and imprinted genes, and all that stuff. And humans keep winding
up being about a halfway between a classic
monogamous pair bonder and a classic
polygamist tournament species. So the basic human version of
it is somewhere in between. But you get variations. You’ve got genetic variations
that either look a little bit more like the monogamous vole
version or the polygamous vole version. And what studies have now
shown– two different studies independently showing this–
have the monogamous vole version. And with the small effect, you
are more likely to get married, you are more likely
to remain married, and both you and
your partner are more likely to rate the
marriage as stable and happy. That’s kind of interesting. Finally, in terms of
the role of vasopressin, in terms of attachment
in males, all of that, and in terms of
social connectiveness, a large body of
studies now have shown mutations in the
vasopressin receptor gene. OK. Anybody want to guess
what disorder you find it? I put that in the
extended notes, haven’t I? People have read it already. I know, I fell for it last time. I am not falling for
that stupid trick again of asking you to prove. He sniffed some oxytocin. So does anybody want to
guess which the– OK. What do you now all
know is there’s now been a lot of
demonstrations of mutations in the vasopressin
receptor gene in family pedigrees with autism, a disease
of very, very little attachment to other humans. So we’ve got written
all over the place here some sort of role of oxytocin
in female attachment formation and vasopressin. And we’ve already
gotten interesting hints that this applies to humans. And we’ve already
gotten interesting hints that individual differences
in the molecular biology of these genes
predicts something about individual differences in
the stability of relationships in humans. OK. So everything we’ve been hearing
about with the neurobiology– and we’re still living in
this part, in this bucket here temporarily– has
been built around heterosexual relationships. What’s known about
the neurobiology of sexual orientation? What has been found is most
strikingly one landmark study, one that got on the
cover of Time magazine, one that had a gigantic,
gigantic impact, which was looking back at
that hypothalamic nucleus, that INAH, I-N-A-H. Yes. Where what we saw
before was very reliably on the average, men, their
size of it is about twice the size as in women. And in other species,
males about twice the size as in females. And a study was
done in the late 80s by a neuroanatomist
names Simon LeVay. LeVay is one of the all-time
great neuroanatomists. He was trained by
Hubel and Wiesel, was a professor at
Harvard Med School for a while before moving
to the Salk Institute. And what he did was
look post-mortem at the brains of a bunch of
individuals where he knew the sexual orientation, men. And what he showed was gay
men, on the average, had this nucleus on the
average was half the size that you saw in
heterosexual men. On the average, it was
about the same size as you saw in
heterosexual women. Amazing landmark study. Everybody learned about
the homosexual brain from this study. Hugely widely reported. And this is kind of interesting. OK. What’s interesting about it? First off, the question you need
to ask is how much variability? Fair amount. It wasn’t all that
reliable of a difference. On the average, it was
about a half the size. Next thing you
would want to know is, has anybody
replicated it since then? Yes. Next thing you
would want to know is, where did LeVay
get the brains from? And these were
predominantly from gay men who had died of AIDS. Is that a confound? Is that going to perhaps
atrophy this part of the brain? Nobody knows. So that remains as a
caveat in that study. What was striking
though was everybody learned about this finding. This became famous. LeVay became extremely
famous for this. And what was also
very interesting about it was the political
context of this finding. A few years before
that, another group had reported another
difference in the hypothalamus based on sexual orientation. And this was– there it is. And what you found was in
this part of the brain, on the average, it would tend
be bigger in women than in men. And what these guys
reported was in gay men, it tended to be bigger
than in straight men. What was puzzling
about the study was this was a part of
a hypothalamus having to do with regulation
of your kidneys. And it was totally ignored
and completely bizarre, except there was
one thing that was done with it, which
was this was viewed as a totally offensive
study in the gay community. This was viewed as an
attempt by scientists to pathologize sexual
orientation, to say, you see, we found something wrong in
the brains of homosexual men. This part of the brain is
bigger than it should be. It’s bigger than
it’s supposed to be. There’s probably two
reasons why that occurred. The first one was that
the scientists who did it were straight. And the second reason being
that they were a Dutch group. And I am willing to
bet unconsciously there was something central European
Nazi echoes of Germanic sounding authors producing
this finding, which there is no shortage of history in
the gay community for being skittish about Nazi
notions of what normality is in human behavior
and human brains. This finding got widely
condemned in the gay community. Out came LeVay with his
finding, and he became the most beloved neuroanatomist ever in
the history of gay communities. One probably important
feature reason for it is that LeVay was
gay, very openly so. Another reason was the part of
the brain he found made sense. It had something to do with
sexual behavior as opposed to the totally puzzling thing. So what was this about? Very interestingly, the
explanation almost certainly is that this was the
part of the hypothalamus next door to the area
that LeVay studied. And if this part were
smaller in gay men simply because of just
physical constraints stuff, this part could get
bigger in gay men. Because this one was
taking up less area. That’s probably
what was going on. What’s really fascinating
though is the political context that this research was done in. And this was that first group,
the senior author of it, a man named Dick Schwab. And he got death threats
because of that study reporting, ooh, here is– easily
interpreted as– something wrong in the brains of gay man. And Simon LeVay became
the hero in the community. This was utterly embraced
by the community. Because in large part,
how it was interpreted as, this is biology. This isn’t choice. This is biology. Look at this. This is ridiculous,
us saying, oh my god. If we have gay teachers
in the classroom, we will turn the Boy Scouts
of America into a gay men. Oh my god, if we have blue-eyed
teachers in the classroom– the usual argument that this is
absolute gibberish to demonize sexual orientation as a choice. Look at this. There’s a neurobiology of it. And this was sufficiently that
I’ve seen people in the Castro District in San Francisco–
this has disappeared somewhat, showing the half life of
neuroanatomical knowledge. But during that time, people
in the Castro District up in the city there, which
is a very gay community, I have seen people with
t-shirts saying– the other term people never really wanted
to embrace this INAH, so its nickname was the
sexually dimorphic nucleus of the hypothalamus. And I have seen people
with t-shirts saying, the only small thing about me is
my sexually dimorphic nucleus. They were actually
selling t-shirts that would say this during
gay pride parades around 1990 or so. Isn’t it great when
people learn neuroanatomy out in the general public there? OK. So an interesting
brain difference confounded by people
who died of AIDS. It’s still not clear
what that means in terms of possibly
negating the finding at least independently replicated. Fascinating piece
of not science, but the political
context of science. This politically incorrect
to an extreme, this very, very widely embraced. One interesting thing is
that paper by LeVay of was published in
the journal Science. Again, constantly mentioned as
probably the most influential science journal in this country. And it was published–
what year was it? ’88. ’88, ’92, ’90? OK. I’m getting the year wrong. But it was just before the
Clinton election against Bush where one of the big issues
was gays in the military. That was the first thing
that Clinton turned to after he was elected. I happen to know the man
who is the editor of Science at the time. And they timed the publication. That paper came out in
late October of that year. And they held it for
that time because they knew that this was going to be
an issue in the election, which was kind of cool that they did
that, although some people may disagree. OK. But we hurtle on. So what other biological,
neurobiological differences, as a function of
sexual orientation? Another one that comes through
over and over and over again, which– what do
you make of this– is apparently there is a
reliable gender difference in the length of
the second finger versus the fourth finger,
the ratio of the two. And just to show how bi–
whoa, did a lot of hands just go up in this auditorium. And just to show how
biologically compelling the explanation is for
it, I don’t actually remember which like– who’s
got the greater four to two ratio, which sex, or whatever. But it is a very–
now people are checking each other’s hands. OK. The first wave of– and now
all this chimp hand inspection stuff happening in here. And what has been shown
quite reliably since then is, on the average, gay men tend
to have the finger length ratio of straight women
rather than of straight men. A small effect there. Another even more
bizarre finding, which is there is something
called the autoacoustic reflex. And what that is is if you sit
there and plug your ears up with your fingers, you will
hear a noise that is just coming from the intrinsic
vibration of something right there in your
ears, and that’s the autoacoustic reflex
generating some low Hertz sound in there. And the rate of the oscillation
differs by sex in humans, which no doubt
explains everything about the tragic
wars of the sexes and why people just don’t
understand each other by gender because of their ears
vibrating at different speeds. But what these studies
have also shown was gay men having the
autoacoustic reflexive vibratory speed more
typical of straight women than straight men. Again, a very small effect. What are all of these about? The assumptions
are it’s got to do with something with prenatal
hormone environment. Stay tuned. We will be coming back to this. Now somewhere in
there you may ask, OK, well what about the neurobiology
of sexual orientation in women? Vastly smaller literature. Far, far less studied. What has been shown so far
are only two endpoints. One is the same deal with the
fourth to second finger ratio. On the average, gay women
have the ratio more typical of straight men
than straight women. The other thing
that’s been shown is the same autoacoustic
reflex thingy going on there. Final realm of
neurobiology, rather than issues of gay versus
straight, what is the neurobiology
of transsexuality? And that used to be
considered to be purely a domain of psychopathology. If being gay used to be
a certifiable psychiatric disorder– up until the early
1970s, the American Psychiatric Association in their textbook,
the Diagnostic Statistical Manual, you could be
psychiatrically certified as ill. A psychiatric disorder was
being homosexual or lesbian. And then in what had to
have been one of the more all-time blow out
committee meetings ever, they decided that,
no, actually it’s not a psychiatric disorder. And overnight, about
40 million Americans were cured of a
psychiatric disease. The notion of transsexuality
as a psychiatric disorder has had much, much
longer shelf life. What’s the neurobiology of that? To date, there have been
a handful of studies, and they show essentially
the same thing– really, really interesting. Another region of
the brain that shows a sex difference in
its average size– don’t even worry about
the name of this. It’s called the bed nucleus
of the stria terminalis. It’s where the amygdala
begins to send its projection into the hypothalamus. Another one to those
gender differences. There is one type
of neuron in there with a certain type of
neurotransmitter, where very, very reliably it is about
twice the size in males than in females. Sufficiently so that
even in human brains, you could pretty confidently
determine the sex of somebody by seeing the number
of these neurons. You’ll see, I’m not
even saying the name of the neurotransmitter. It’s irrelevant. It’s just another one
of those differences, a dimorphism in a region of
the brain, a really, really reliable one. And this was a study done by
some superb neuroanatomists looking at transsexuals. And what they showed
was very interesting, which was very, very reliably
and a very powerful effect. What you would see
in their large sample size of transsexuals
brains post-mortem was people would have this
part of the brain, the size not of their sex that they were
born with, but rather of the sex they insisted they
always actually were. Wow. Immediate questions
one must ask. OK. Well, maybe this
is due to the fact that when people change
gender, transsexual procedures, there’s a whole lot
of hormones involved. And maybe that’s doing something
to this part of the brain. Critical control
that they had was this was looking
both at transsexuals who had made gender changes and
those who went to their death bed saying this is
not the sex that I am, I got the wrong body, but
never made the change. It wasn’t a function
of having actually gone through the transition
and the endocrine manipulations with it. Another control
they had, which was looking at men who would get
a certain type of testicular cancer where they
would have to be treated with certain
feminizing hormones. In other words, very similar
to some of the endocrine treatments of male-to-female
transgendered individuals. And post-mortem, you didn’t
see the changes there. It has nothing to do
with the hormones. It had to do with the person
insisting from day one that they got the wrong body. And this was a landmark
study, fabulously well done and controlled,
and replicated once since then showing that
what transsexualism used to be thought of
is that people who think that they’re a different
gender than they actually are. What this study suggests is
what transsexualism is about is people who got the
wrong gendered body. And these are people who are
chromosomally of one sex. In terms of their gonads,
they’re of that sex. In terms of their hormones,
they’re of that sex. In terms of their genitalia
and their secondary sexual characteristics,
they are of that sex. But they’re insisting,
that’s not who I really am. This part of the brain
agrees with them. Also very interestingly
that study was done by the same Dutch
scientists who did this one. Again, this is very
complex terrain in terms of what these
things wind up implicating. Interestingly, that study was
published right around the time that the city of San Francisco
did something very cool, which was for city employees
now, medical insurance will cover transgender
operations. However, there is no evidence
that the obscure endocrine journal published out
of Latvia or something did that like the afternoon
before the San Francisco commissioners had their
meeting on that one. But nonetheless,
this is a subject with all sorts of
realms of implications. One additional study
about transsexualism. OK. How many of you know about
Phantom Limb Syndrome? OK. You are a guy with a penis,
and you get a certain type of penile cancer. And what’s often done is
your penis is excised. It is cut off. And about 60% of men who have
had to have their penises removed because of
cancer there wind up getting phantom penile
sensations, which I don’t want to know about. What you see though is when you
take transgendered individuals who go from male to
female, in other words, as part of it having
their penises removed, 0% rate of penile
phantom sensation. Suggestion being that there
is something much more “normal” in that case than
when a penis is being removed for cancer, a whole new area
of research, very novel, very challenging. OK. So this has giving us a
sense now of this bucket. And we are now ready to move
on to, what in the environment releases some of
these fixed action patterns of sexual behavior? What in the environment
is doing this or that to the medial preoptic
area or the amygdala or vasopressin receptor
levels or any such thing. What are the sensory
triggers for the neurobiology of sexual behavior? OK. Right off, what is obvious is
we are in ethologyville here. It’s going to depend on the
species which sensory modality is most important. And this is, once again, the
crushing of the limbic system equals nose-brain concept. Limbic system equals
nose-brain if you are a rat. It’s, once again, going
to be interviewing an animal in its own language. You’ve got species where
the releasing stimuli are all visual. And we’ve heard one
example of that already, which were the pathetic male
turkeys getting faked out by the Styrofoam female turkeys
with the feathers pointing the wrong way. Visual stimuli. Other species are
quite visual as well. Primates, non-human primates,
monkeys, for example. And what studies have shown
is– how’s this for remarkable? OK. Here we have– nah, forget it. OK. You will take a rhesus
monkey, a rhesus monkey from a social group. And he’s sitting there,
and he can lever press for various rewards. And he will press a lever
a certain number of times to get some juice as a reward. He will press a lever a
certain number of times to see a high ranking male
from his social group, no doubt to keep
an eye on the guy. He will not lever press
to see a male who is lower ranking than him, but
he will lever the most to see pictures of female
rhesus monkeys who are in heat. Whoa! Is that weird or what? And the bigger the estrus
swelling on the female, the more levered
pressing the male will do to be able to see this. So that’s kind of interesting. And this close relative of ours,
in terms of visual stimuli. What is also known
is humans are highly visual in their sexual
responsiveness as well. Visual stimuli as
releasing stimuli. What is no surprise
whatsoever is on the average, males are more responsive
to visual releasing stimuli than are females among humans. And this has been
shown in various ways. For example, now studies using
brain imaging showing that for visually sexually arousing
material that not only are men on the average
subjectively more responsive, but you get more
of an activation of the dopamine pathways
in men than in women. What’s interesting also
is that in men, you uniquely get activation of that
area of the amygdala as well. And again, that weird world
of the structure of the brain heavily involved in aggression
also being involved something about male sexual motivation. What else? Then there, of course, is the
world of tactile stimulation. And what you’ve got is a whole
domain where, not surprisingly, stimulate the right
tactile receptors, and it is sexually arousing. Are they sure? Have they done enough
research on this? And you will activate
dopamine regions. All of that making
perfect sense. What also makes perfect sense is
some types of tactile receptors in some part of the body
activate dopamine more than other types. We are now in the whole
world of erogenous zones and that whole deal. What is also clear is
that these receptors, these tactile receptors, their
responsiveness to stimuli will change depending
on your hormone levels. And what you see is in women,
tactile responsiveness, the extent to which
tactile stimulation of skin throughout the body, but
especially of the genitals, tactile stimulation evokes
more dopamine activation when somebody is ovulating. In other words, at
ovulation, women’s skin is more sensitive to
sexually arousing touch. In men, it requires
testosterone. Men who are castrated, tactile
responsiveness to stimuli goes down in terms of
finding them pleasurable, sexually arousing. Final domain of tactile
stuff, the specialized version we’ve heard of already, that
lordosis reflex business. Again, that’s a spinal
reflex, but this is not a spinal reflex of bopping
somebody on the knee and their leg goes flying out. This is spinal
reflex where you only get the lordotic arch backing
in females– arch backing? Back arching. OK. You don’t get either,
but you especially don’t get the arch
backing when you don’t have elevated estrogen levels. Only when females are ovulating
are those tactile receptors sensitive to pressure on
the flanks of the rear end, and out comes the reflex there. So tactile stimulation. At the end of the day,
though, without question, as agreed upon by every
scientist on earth, the coolest sensory modality
for sexual release stimuli are olfactory cues, pheromones. And thus, we enter the
magnificent wonderful world of pheromonal communication
and pheromonal sexual arousal. All sorts of interesting
findings there. First, at the end of
generating pheromones that are sexually arousing. What is required in both
species– in both species? Whoa. That was an interesting slip. What’s required in
both sexes– OK. What’s required in both kinds
is the right hormones into order to generate pheromones. Sexually arousing pheromones
in all the different species look– that’s where
the species part was coming into that sentence. What you see is males do not
generate sexually arousing pheromones if they lack
testosterone levels. Ovariectomized females,
women, rats, monkeys, et cetera, who have had
their ovaries removed do not produce pheromones
that are sexually arousing. What that of course
brings up is, what are some of the chemical
constituents of pheromones? And this is very interesting
because it brings up another one of those weird
domains of neuromarketing, pheromones that have
sexually arousing components. There’s all sorts of fatty
acids that play a role in that. But a lot of what is sexually
arousing about pheromones in different species
are breakdown products of sex hormones. Breakdown products of
androgens in males, of estrogens in females. And that winds of providing
some of these sexually arousing aspects of those odors. What does that
immediately tell you? Your olfactory receptors have
all sorts of receptors there that could pick up on remnants
of testosterone and estrogen, things of that sort. That makes a lot of sense. What doesn’t make
any sense at all is the following finding,
which is perfume. Perfume, in its classic
form, is made out of the sweat of various animals. OK. Except we’re going to get into
even worse domain here, which is perfumes
traditionally, before getting the synthetic
versions, were typically made from the sweat
of male animals. Hm. What’s that about? Musk. Things of that sort. Chanel No. 5 is made from the sweat of
whipped male Abyssinian cats. I kid you not. And this even produced
protests some years ago, animal rights groups,
about how we should not be perfuming ourselves
with the sweat of whipped male Abyssinian cats. Suddenly, you’ve
got a real puzzle. Along comes synthetic perfumes,
and the majority of them are made of synthetic
versions of androgens. Wait a second. Perfume is made up of all
sorts of breakdown products of male sweat. Isn’t perfume supposed to
like smell good to guys? We have a deep
abiding puzzle here. And there is an answer for it. Let me survey people first off. OK. Guys in the room,
how many of you basically think that
most perfumes smell kind of appealing? OK. How many of you don’t? OK. Females, how many of you think
your basic off-the-rack perfume smells appealing? OK. Well, that proves something. OK. Just complete it, how
many of you don’t? OK. The vast majority of perfumes
are not purchased by men. The vast majority are
purchased by women. In other words, most of
the marketing decisions about what to stick
in your perfumes are being marketed
for people who are going to decide if
it’s appealing or not, people who have lots of
estrogen in their bloodstream rather than androgens. That is thought to be
the explanation for how it is that most perfumes are
derived from male pheromones. Yeah. The other thing is if
I were to wear perfume it would more so that girls
think I smell good instead of for me to think I smell god. OK. Yes. The strategizing starts. OK. So a whole new world of
potential neuromarketing here. But this taps into, what are
the chemical constituents of pheromones? What sort of
information is carried by pheromones, olfactory
communication, between genders? It will tell you the
species of the individual. It will tell you their gender. It will tell you whether
they are gonadally intact, whether they’ve been
castrated or not. It will tell you something
about their health. It will tell you whether
they are terrified or not. Have the sweat from someone or
something that is terrified, and as we already know,
it will smell differently to the amygdala. It will have a lot more
glucocorticoid breakdown products in it. And it will tell you,
as we know already, if it’s the right species, if
this person is related to you. Final point before we then
go into the specifics of what pheromones are doing to the
neurobiology of all this, finally, not only do you need
to have hormones intact in order to generate the
pheromones, you need to have the right
reproductive hormones on board in order to perceive them. Men who are castrated
no longer find the smells of
female ovarian– OK, I’m getting ahead
of myself here. OK. If you don’t have the
hormones on board, if you have no estrogen
and you’re female, or if you have no
testosterone and you are male, you will not be
able to distinguish the sweat of women and men. Gonadally intact people can
at above the chance level. Finally, women become
far better at detecting the smell of– distinguishing
the smell of men versus women when they are ovulating. Finally, finally,
that’s not what you see when you have gay individuals. Gay men are better at
detecting the smell of gay men than either straight
men or straight women. So we’ve gotten the
first pieces of here with the pheromonal system. You have to be hormonally
intact to generate pheromones that are sexually
informative and to detect them. What we will then transition
to is, what sort of information is being carried
in the pheromones and what effect does it
have on the neurobiology of depending on who’s
pheromones you are sniffing? OK. So we will– For more, please visit
us at stanford.edu.

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