Re: Is Romantic Love Hardwired Into Our Brains?
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Re: Is Romantic Love Hardwired Into Our Brains?         

Group: alt.philosophy · Group Profile
Author: Immortalist
Date: Jan 9, 2007 19:37

Anthony Campbell wrote:
> On 2007-01-08, Immortalist yahoo.com> wrote:
>> "It became apparent to me that
>> romantic love was a drive -- a
>> drive as strong as thirst,
>> as hunger..." --Helen Fisher
>>
>> If romantic passion is hardwired into our brains by millions of years
>> of evolution, it is not an emotion; it is a drive as powerful as
>> hunger.
>>
>> Anthropologist Fisher argues that much of our romantic behavior is
>> hard-wired in [her] provocative examination of love. Her case is
>> bolstered by behavioral research into the effects of two crucial
>> chemicals, norepinephrine and dopamine, and by surveys she conducted
>> across broad populations.
>>
>
> Doesn't she discuss oxytocin and vasopressin, which are currently
> attracting a lot of attention in this field.
>
> Prarie voles are monogomous, with both parents rearing the pups.
> Montane voles are promiscuous and the females are less solicitous about
> their pups. Both species have receptors in their brains for oxytocin and
> vaasopressin; oxytocin causes attachment in females, vasopressin does so
> in males.
>

Actually she doeas talk quite a bit about oxytocin and vasopressin but
her main focus is upon iMRI scans of active parts of the brain. This is
opening up into an entre new area of research.

But now that you mention it, I remember reading in one of these books
about how these molecules came about for some other use and then were
appropriated by natural selection for other abilities. Oh, ya, I
remember which book now;

NATURE VIA NURTURE - genes, experience, and what makes us human
http://www.amazon.com/exec/obidos/tg/detail/-/0060006781/

...A working hypothesis is that oxytocin released during mating
activates those limbic sites rich in oxytocin receptors to confer some
lasting and selective reinforcement value on the mate.

Or, to put it more poetically, you fall in love.

What is this oxytocin and why does Insel make such an extravagant claim
for it? The story starts with an almost ridiculously unromantic
process: urination. Some 400 million years ago, when the ancestors of
our species first left the water, they were equipped with a tidy little
hormone called vasotocin, a miniature protein made out of a chain of
just nine amino acids formed into a ring. Its job was to regulate the
balance of salt and water in the body, and it performed this job by
rushing about switching on cells in the kidney or other organs. Fish
still use two different versions of vasotocin for this purpose today,
and so do frogs. In the descendants of reptiles-and that includes human
beings-there are two slightly different copies of the relevant gene
lying next to each other, facing different ways (in human beings on
chromosome 20). The result today is that all mammals have two such
hormones, called vasopressin and oxytocin, that differ at two of the
links in the chain.

These hormones still do their old job. Vasopressin tells the kidney to
conserve water; oxytocin tells it to excrete salt. But, like vasotocin
in modern fish, they also have a role in the regulation of reproductive
physiology. Oxytocin stimulates the contraction of muscles in the womb
during birth; it also causes milk to be expelled from the ducts in the
breast. The GOD is an economizer: having invented a switch for one
purpose, he readapts it for other purposes, by expressing the oxytocin
receptor in a different organ.

An even greater surprise came in the early 1980s, when scientists
suddenly realized that vasopressin and oxytocin had a job to do inside
the brain as well as being secreted from the pituitary gland into the
bloodstream.

So they tried injecting oxytocin and vasopressin into the brains of
rats to see what the effect would be. Bizarrely, a male rat injected
with intracerebral oxytocin immediately begins yawning and
simultaneously gets an erection. So long as the dose is low, the rat
also becomes more highly sexed: it ejaculates sooner and more
frequently. In female rats, intracerebral oxytocin induces the animal
to adopt a mating posture. In human beings, meanwhile, masturbation
increases oxytocin levels in both sexes. All in all, oxytocin and
vasopressin in the brain seem to be connected to mating behavior.

All this sounds rather unromantic: urine, masturbation, breast
feeding-hardly the essence of love. Be patient. In the late 1980s, Tom
Insel was working on the effect of oxytocin on maternal behavior in
rats. Brain oxytocin seemed to help the mother rat form a bond with her
young, and Insel identified the parts of the rat brain that were
sensitive to the hormone. He switched his attention to the pair bond,
wondering if there were parallels between a female's bond to her young
and the bond to her mate. At this point he met Sue Carter, who had
begun to study prairie voles in the laboratory. She told him that the
prairie vole is a rarity among mice for its faithful marriages. Prairie
voles live in couples, and both father and mother care for the young
for many weeks. Montane voles, on the other hand, are more typical of
mammals: the female mates with a passing polygamist, separates quickly
from him, bears young alone, and abandons them after a few weeks to
fend for themselves. Even in the laboratory, this difference is clear:
mated prairie voles stare into each other's eyes and bathe the babies;
mated montane voles treat their spouses like strangers.

Insel examined the brains of the two species. He found no difference in
the expression of the two hormones themselves, but a big difference in
the distribution of molecular receptors for them-the molecules that
fire up neurons in response to the hormones. The monogamous prairie
voles had far more oxytocin receptors in several parts of the brain
than the polygamous montane voles. Moreover, by injecting oxytocin or
vasopressin into the brains of prairie voles, Insel and his colleagues
could elicit all the characteristic symptoms of monogamy, such as a
strong preference for one partner and aggression toward other voles.
The same injections had little effect on montane voles, and the
injection of chemicals that block the oxytocin receptors prevented the
monogamous behavior. The conclusion was clear: prairie voles are
monogamous because they respond more to oxytocin and vasopressin.

In a virtuoso display of scientific ingenuity, Insel's team has gone on
to dissect this effect in convincing detail. They knock the oxytocin
gene out of a mouse before birth. This leads to social amnesia: the
mouse can remember some things, but it has no memory of mice it has
already met and will not recognize them. Lacking oxytocin in its brain,
a mouse cannot recognize mice it met 10 minutes before-unless those
mice were "badged" with a nonsocial cue such as a distinctive lemon or
almond scent (Insel compares this situation to that of an absent-minded
professor at a conference who recognizes friends by their name tags,
not their faces). Then by injecting the hormone into just one part of
the animal's brain-the medial amygdala-in later life the scientists can
restore social memory to the mouse completely.

In another experiment, using a specially adapted virus, they turn up
the expression of the vasopressin receptor gene in the ventral
pallidum, a part of a vole's brain important for reward. (Pause here to
roll that idea around your mind a few times to appreciate just what
science can do these days: scientists use viruses to turn up the
volumes of genes in one part of the brain of a rodent. Even 10 years
ago such an experiment was unimaginable.) The result of turning up the
gene's expression is to "facilitate partner preference formation,"
which is geekspeak for "make them fall in love." They conclude that for
a male vole to pair-bond, it must have both vasopressin and vasopressin
receptors in its ventral pallidum. Since mating causes a release of
oxytocin and vasopressin, the prairie vole will pair-bond with whatever
animal it has just mated with; the oxytocin helps in memory, the
vasopressin in reward. The montane vole, by contrast, will not react in
the same way, because it lacks receptors in that area. Female montane
voles express these receptors only after giving birth, so they can be
nice to their babies, briefly.

So far I have talked of oxytocin and vasopressin as if they were the
same thing, and they are so similar that they probably stimulate each
other's receptors somewhat. But it appears that to the extent that they
do differ, oxytocin makes female voles choose a partner; vasopressin
makes males choose a partner. When vasopressin is injected into the
brain of a male prairie vole, he becomes aggressive toward all voles
except his mate. Attacking other voles is a (rather male) way of
expressing love.

All this is astonishing enough, but perhaps the most exciting result to
emerge from Insel's laboratory concerns the genes for the receptors.
Remember that the difference between the prairie vole and the montane
vole lies not in the expression of the hormone but in the pattern of
expression of the hormone's receptors. These receptors are themselves
products of genes. The receptor genes are essentially identical in the
two species, but the promoter regions, upstream of the genes, are very
different. Now recall the lesson of chapter 1: that the difference
between closely related species lies not in the text of genes
themselves but in their promoters. In the prairie vole, there is an
extra chunk of DNA text, on average about 460 letters long, in the
middle of the promoter. Insel's team made a transgenic mouse with this
expanded promoter, and it grew up with a brain like a prairie vole's,
expressing vasopressin receptors in all the same places, though it did
not form a pair bond. Steven Phelps then caught 43 wild prairie voles
in Indiana and sequenced their promoters: some had longer insertions
than others. The insertions varied from 350 to 550 letters in length.
Are the long ones in more faithful husbands than the short ones? Not
yet known.

The conclusion to which Insel's work is leading is devastating in its
simplicity. The ability of a rodent to form a long-term attachment its
sexual partner may depend on the length of a piece of DNA text in the
promoter switch at the front of a certain receptor gene. That in turn
decides precisely which parts of the brain will express the gene, Of
course, like all good science, this discovery raises more questions
than it settles. Why should feeding oxytocin receptors in that part of
the brain make the mouse feel well-disposed toward its partner? It is
possible that the receptors induce a state a bit like addiction, and in
this respect it is noticeable that they seem to link with the D2
dopamine receptors, which are closely involved in various kinds of drug
addiction. On the other hand, without oxytocin, mice cannot form social
memories, so perhaps they simply keep forgetting what their spouse
looks like.

Mice are not men. You know by now that I am about to start
extrapolating anthropomorphically from pair-bonding in voles to love in
people, and you probably do not like my drift. It sounds reductionist
and simplistic. Romantic love, you say, is a cultural phenomenon,
overlaid with centuries of tradition and teaching. It was invented at
the court of Eleanor of Aquitaine, or some such place, by a bunch of
oversexed poets called troubadours; before that there was just sex.

Even though in 1992 William Jankowiak surveyed 168 different
ethnographic cultures and found none that did not recognize romantic
love, you may be right. I certainly cannot prove to you-yet-that people
fall in love when their oxytocin and vasopressin receptors get tingled
in the right places in their brains. Yet. And there are cautionary
hints about the dangers of extrapolating from one species to another:
sheep seem to need oxytocin to form maternal attachment to their young;
mice apparently do not. Human brains are undoubtedly more complicated
than mouse brains.

But I can draw your attention to some curious coincidences. A mouse
shares much of its. genetic code with a human being. Oxytocin and
vasopressin are identical in the two species and are produced in the
equivalent parts of the brain. Sex causes them to be produced in the
brain in both human beings and rodents. Receptors for the two hormones
are virtually identical and are expressed in equivalent parts of the
brain. Like those of the prairie vole, the human receptor genes (on
chromosome 3) have a-smaller-insertion in their promoter regions. As
with the prairie voles of Indiana, the lengths of those promoter
insertions vary from individual to individual: in the first 150 people
examined, Insel found 17 different lengths. And when a person who says
she (or he) is in love contemplates a picture of her loved one while
sitting in a brain scanner, certain parts of her brain light up that do
not light up when she looks at a picture of a mere acquaintance. Those
brain parts overlap with the ones stimulated by cocaine. All this could
be a complete coincidence, and human love may be entirely different
from rodent pair bonding, but given how conservative the GOD is and how
much continuity there is between human beings and other animals, you
would be unwise to bet on it.

Shakespeare was ahead of us, as usual. In A Midsummer Night's Dream,
Oberon tells Puck how Cupid's arrow fell upon a white flower (the
pansy), turning it purple, and that now the juice of this flower

... on sleeping eyelids laid
Will make or man or woman madly dote
Upon the next live creature that it sees.

Puck duly fetches a pansy, and Oberon wreaks havoc with the lives of
those sleeping in the forest, causing Lysander to fall in love with
Helena, whom he has previously scorned; and causing Titania to fall in
love with Bottom the weaver wearing the head of an ass.

Who would now wager against me that I could not soon do something like
this to a modern Titania? Admittedly, a drop on the eyelids would not
suffice. I would have to give her a general anesthetic while I
cannulated her medial amygdala and injected oxytocin into it. I doubt
even then that I could make her love a donkey. But I might stand a fair
chance of making her feel attracted to the first man she sees upon
waking. Would you bet against me? (I hasten to add that ethics
committees will-or should-prevent anybody taking up my challenge.)

I am assuming that, unlike most mammals, human beings are basically
monogamous like prairie voles, and not promiscuous like montane voles.
I base this assumption on the argument enunciated in chapter 1
concerning the size of testicles; on the ample evidence from
ethnography that, though most human societies allow polygamy, most
human societies are still dominated by monogamous relationships; and on
the fact that human beings usually practice some paternal care-a
characteristic feature of the few mammal species that live as social
monogamists. Furthermore, as we have liberated human life from economic
and cultural straitjackets, such as arranged marriage, we have found
monogamy growing more dominant, not less. In 1998 the most powerful man
in the world, far from treating himself to a gigantic harem, got into
trouble for having an affair with one intern. The evidence is all
around you for long-term and exclusive (but sometimes cheated-on) pair
bonds as the commonest pattern in human relationships.

Chimpanzees are different. Long-term pair bonds are unknown among them,
and I predict that they have fewer oxytocin receptors in the relevant
parts of their brains than human beings, probably as a result of having
shorter gene promoters.

The story of oxytocin lends at least tentative support to William
James's notion that love is an instinct, evolved by natural selection,
and is part of our mammal heritage, just like four limbs and 10
fingers. Blindly, automatically, and untaught, we bond with whoever is
standing nearest when the oxytocin receptors in the medial amygdala get
tingled. One sure way to tingle them is to have sex, although
presumably chaste attraction can also do the trick. Is this why
breaking up is hard to do?

Having oxytocin receptors does not make it inevitable that somebody
will fall in love during his life, nor predictable when it will happen,
or with whom. As Niko Tinbergen, the great Dutch ethologist,
demonstrated in his studies of instincts, the expression of a fixed,
innate instinct must often be triggered by an external stimulus. One of
Tinbergen's favorite species was the stickleback, a tiny fish. Male
sticklebacks become red on the belly in the breeding season, when they
defend small territories in which they build nests, which attract
females. Tinbergen made little models of fish and caused them to
"invade" the territory of a male fish. A model of a female elicited the
courtship dance of the male, even if the model was astonishingly crude;
so long as it had a "pregnant" belly, it excited the male. But if the
model had a red belly, it would trigger an attack. It could be just an
oval blob with a crudely drawn eye but no fins or tail: still it was
attacked just as vigorously as if it were a real male rival-so long as
it was red. One of the legends of Leiden, where Tinbergen first worked,
is that he noticed his sticklebacks would threaten the red post-office
vans that drove past the window.

Tinbergen went on to demonstrate the power of these "innate releasing
mechanisms" to provoke the expression of an instinct in other species,
notably the herring gull. Herring gulls have a yellow beak with a
bright red spot near the tip. The chicks peck at this spot when begging
for food. By presenting newborn chicks with a series of models,
Tinbergen demonstrated that the spot was a powerful releaser for the
begging action, and the redder it was the more powerful it was. The
color of the beak or the head of the bird mattered not at all. So long
as there was a contrasting spot near the tip of the bill, preferably in
red, it would elicit pecking. In modern jargon, scientists would say
that the chick's instinct and the adult's beak spot had "coevolved." An
instinct is designed to be triggered by an external object or event.
Nature plus nurture.

The significance of Tinbergen's experiments was that they revealed just
how complex instincts could be, and yet how simply triggered. The
digger wasp Tinbergen studied would dig a burrow, go and catch a
caterpillar, paralyze it with a sting, bring it back to the burrow, and
deposit it with an egg on top, so that the baby wasp could feed on the
caterpillar while growing. All this complex behavior, including the
ability to navigate back to the burrow, was achieved with almost no
learning, let alone parental teaching. A digger wasp never meets its
parents. A cuckoo migrates to Africa and back, sings its song, and
mates with one of its own species without, as a chick having ever seen
either a parent or a sibling.

The notion that animal behavior is in the genes once troubled
biologists as much as it now troubles social scientists...

NATURE VIA NURTURE - genes, experience, and what makes us human
http://www.amazon.com/exec/obidos/tg/detail/-/0060006781/
> By manipulating the number of receptors you can convert a prarie vole to
> behave like a montane vole or vice versa. The number of receptors in a
> given vole's brain predicts how likely it is to bond.
>
> Both hormones act on the nucleus accumbens at the base of the brain, the
> so-called reward centre.
>
> Anthony
>
>
>
> --
> Anthony Campbell - ac@acampbell.org.uk
> Microsoft-free zone - Using Linux Gnu-Debian
> http://www.acampbell.org.uk (blog, book reviews,
> on-line books and sceptical articles)
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